Multiple Sclerosis (MS)

Management Team

Multiple Sclerosis (MS)

Overview

MS is an inflammatory demyelinating disorder of the central nervous system (CNS). MS occurs rarely before puberty and after the age of 60 years. Peak incidence occurs between 30 and 40 years of age. The episodes are often triggered by smoking, deficiency of vitamins D or B12, and higher altitudes.

  • Exact cause is unknown
  • May be attributed to a combination of environmental and genetic factors

  • Genetics: A gene on chromosome 6p21 is associated with MS, and about 200 genes contribute to the MS risk
  • Family history
  • Female sex 
  • Age range 20 to 40 years
  • Race: White people, especially those from Northern Europe, are at the highest risk.
  • Climate: MS is more common in temperate climates, such as Canada, the northern United States, and Europe
  • Low vitamin D levels
  • Obesity
  • Smoking; second-hand smoke exposure may be related to the risk of paediatric MS.
  • Epstein-Barr virus (EBV)
  • Gut dysbiosis

Symptoms depend on the structure involved in neuraxis

  • Transverse myelitis
    • Weakness, sensory symptoms
    • Urinary urgency and retention
    • Flexor spasms
    • Spastic quadra or paraparesis
    • Sensory level
  • Brainstem
    • Ataxia
    • Diplopia
    • Dysarthria
    • Facial numbness
    • Internuclear ophthalmoplegia
    • Gaze palsy
    • Rubral tremor
  • Cerebellum
    • Ataxia
    • Dysarthria
    • Nystagmus
  • Optic neuritis
    • Visual loss
    • Painful eye movements
    • RAPD (relative afferent pupillary defect)
    • Impaired colour vision (Ishihara colour plates)
    • Decreased acuity
    • Optic atrophy
  • Cerebral hemispheres:
    • Poor memory
    • Disinhibition
    • Dementia
    • Epilepsy (rarely)
    • Lhermitte’s symptom (Neck flexion causes current like sensation or tingling)
    • Uhtoff’s phenomenon, which is worsening of symptoms, e.g. vision, when body temperature is raised due to hot shower or exercise
    • Internuclear ophthalmoplegia (impaired adduction on abducting the other eye)

85% of patients experience relapse or disease remittance (RRMS), 50–60% experience the secondary progressive phase (SPMS), and 10% have primary progressive disease (PPMS) with gradual accumulation of disability.

  • MRI to determine T2W high signal changes in the corpus callosum, periventricular white matter, and brainstem
  • McDonald criteria
  • Evoked responses evaluation:
    • Visual evoked responses (VER): delayed even after the recovery of optic neuritis
    • Somatosensory evoked potentials (SSEP)- delayed in cases of spinal cord lesions.

Neurologist

  • Corticosteroids
  • Disease-modifying therapy (DMT) : Interferons, Glatiramer acetate, Monoclonal antibodies natalizumab, rituximab, alemtuzumab
  • Supportive treatment for spasticity, bladder dysfunction, fatigue
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Multifocal Motor Neuropathy with Conduction Blocks (MMNCB)

Management Team

Multifocal Motor Neuropathy with Conduction Blocks (MMNCB)

Overview

MMNCB is an autoimmune neuropathy affecting middle-aged males causing weakness in a specific nerve distribution. It results in sequential weakness of different parts of limbs.

It is caused due to generation of autoantibodies (anti GM1), which damage the nerve fibres and leads to failure of conduction of nerve impulse.

It is a rare disorder and the risk factors are not known.

  • Weakness and atrophy of hands and legs, hand grip weakness, wrist and foot drop
  • Distal involvement
  • No sensory symptoms

Neurologist

  • Clinical signs and symptoms
  • NCV: demonstration of conduction block (>50% decrease in amplitude of motor unit across proximal and distal stimulation)
  • Nerve biopsy (rarely needed)
  • Blood tests for anti GM1 antibodies

  • Immunomodulation using intravenous immunoglobulins. Other immunomodulators such as cyclophosphamide, or rituximab may also be used
  • Rehabilitation using orthosis and assistive devices
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Diabetic Retinopathy

Management Team

Diabetic Retinopathy

Overview

Diabetic retinopathy, a common complication associated with diabetes, refers to high blood sugar-induced damage to the retina, which comprises layers of light-detecting cells. If left untreated, diabetic retinopathy can cause blindness. However, the progression of diabetic retinopathy to the visual impairment stage takes a long time.

Over time, excess sugar in the blood causes the blockage of the tiny blood vessels nourishing the retina. This results in the blood supply to the retina to be cut off. Angiogenesis (the growth of new blood vessels) often serves a natural strategy to counter loss of blood vessels. However, the improper development of these new blood vessels causes them to spring leaks. Diabetic retinopathy can be categorised into two main types each with distinct causes:

  • Early diabetic retinopathy: This is a common form. In this condition, new blood vessels are not growing (proliferating). Thus, this condition is also called non-proliferative diabetic retinopathy (NPDR). In NPDR, the walls of the blood vessels in your retina weaken, causing the protrusion of tiny bulges from the walls of the smaller vessels. Sometimes, these bulges may cause the leakage of blood and fluid into the retina. Although this condition is unlikely to affect vision, it can progress to a state at which it is sight threatening. Mild NPDR and moderate-to-severe NPDR (the condition worsens, owing to increased bleeding into the retina) increase the risk of vision loss in the future.
  • Advanced diabetic retinopathy: In some cases, diabetic retinopathy progresses to this severe type (also called proliferative diabetic retinopathy; PDR). PDR is accompanied by diabetic macular oedema. In PDR, blood vessels in the retina are blocked, resulting in a loss of blood supply. This promotes abnormal angiogenesis in the retina. Scar tissue formation resulting from the growth of these fragile blood vessels and the leakage of blood from these vessels into the vitreous humour (the clear, jellylike substance in the central part of the eye) lead to retinal detachment, increased intraocular pressure, optic nerve damage, and vision loss. Although the peripheral vision is not affected, without treatment, patients may be unable to perform daily activities, such as reading or driving.

Regular diabetic retinopathy screening is important because symptoms are not always noticeable until the condition has progressed to a serious stage. The early signs of diabetic retinopathy can be detected during these routine eye tests. This will aid the administration of the correct treatment to ensure that vision loss does not occur.

Diabetic retinopathy can also cause other symptoms:

  • Gradual deterioration of vision, including blurry or patchy vision.
  • Sudden vision loss.
  • Redness or pain in the eye.
  • Eye floaters.

Comprehensive dilated eye examinations are often the best method to diagnose diabetic retinopathy. In this examination, the pupils are widened (dilated) via the administration of specialised drops so that the ophthalmologist has a clear view of the regions within the eyes. These drops often cause the blurring of vision, but their effects wear off in a few hours. The ophthalmologist will examine different parts of the eyes for abnormalities using the following techniques:

  • Fluorescein angiography: After the eyes are dilated, the dye fluorescein is injected into a vein (in the arm). Images are captured as the dye circulates through the ocular blood vessels. These images help identify broken, leaky, or closed blood vessels.
  • Optical coherence tomography (OCT): Cross-sectional images of the retina are obtained. These images help the doctors ascertain the retinal thickness, enabling the determination of the extent of fluid leakage into the retinal tissues.

Diabetic retinopathy treatment is required only if notable problems are detected during screening. Preventive measures to lower the risk include:

  • Diabetes treatment (controlling blood sugar, pressure, and cholesterol and regular intake of diabetes medication).
  • Maintaining a healthy lifestyle.
  • Regular eye examinations.

However, for advanced-stage diabetic retinopathy, specific treatments may be required. These include:

  • Laser photocoagulation for patients with diabetic macular oedema. Small laser burns are introduced in the damaged areas of the retina to reduce fluid leakage. While this treatment may not result in notable vision improvement, it does help suppress further deterioration of vision.
  • Injection of anti-VEGF drugs into the eye.
  • Surgical procedures for scar tissue removal and elimination of blood leaking into the eye may be needed for patients with severe diabetic retinopathy.
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Conjunctivitis

Management Team

Conjunctivitis

Overview

The conjunctiva is the transparent membrane that lines the eyelids and eyeballs and protects the white part of the eye and the areas under the eyelids. Conjunctivitis, also known as pink eye, refers to the inflammation of the conjunctiva.

Based on the causative agents, there are different types of conjunctivitis:

  • Viral conjunctivitis: Acute (short-term) conjunctivitis is most commonly caused by viruses, especially those belonging to the adenovirus family. Several other viruses, such as the measles or mumps viruses, viruses that cause eye herpes, enteroviruses or coxsackieviruses (cause hand, foot, and mouth disease) (uncommon), or SARS-CoV-2 (causes COVID-19) (uncommon), can also cause pink eye. Viral conjunctivitis tends to cause watering and redness of the eyes and can persist for two to three weeks even after appropriate treatment. Usually, viral conjunctivitis does not affect vision. In rare cases, it may cause the blurring of vision or a glares when looking directly at bright objects. This is due to an inflammatory reaction that results in the formation of small white dots on the cornea (the transparent front layer of the eye). These spots usually go away after a few weeks or sometimes, a few months.
  • Bacterial conjunctivitis: Bacteria are the second most common causes of infectious conjunctivitis. The most common bacteria that cause conjunctivitis are Staphylococcus species (which cause staph infections), Streptococcus species (which cause strep throat and pneumococcal disease), Haemophilus influenzae (which causes meningitis in young children), and bacteria that cause sexually transmitted infections, such as chlamydia, gonorrhoea, and syphilis. Moreover, these conditions may also be passed from the mother to child, leading to neonatal conjunctivitis, a condition that can cause permanent blindness and/or permanent eye damage. Bacterial conjunctivitis is associated with redness in the eyes along with a sticky yellow discharge.
  • Allergic conjunctivitis: Sometimes, the immune system reacts to usually harmless substances like pollen, dust, or grass, causing a non-infectious type of conjunctivitis. This is common in patients with pre-existing allergies or a family history of allergies. The occurrence of seasonal allergic conjunctivitis varies depending on the season and weather conditions. Individuals with pre-existing allergies (e.g., allergies to dust mites, dander (animal fur), and pollen) may display symptoms throughout the year.
  • Other types of non-infectious conjunctivitis: Apart from allergens, other factors/substances may cause conjunctivitis, such as toxic substances or eye irritants (including contact lenses or contact solution, cosmetics or eye products (shampoos and eye makeup), chlorine in swimming pools, smoke, and certain types of medications), injuries that cause conjunctival damage, immune disorders that affect the eye, and conjunctival tumours or cancers.

Infective conjunctivitis can affect one eye or both eyes. Its symptoms include:

  • Inflammation and redness of the whites of the eyes.
  • Gritty, watery, or sticky eyes, especially in the mornings.
  • Blurred vision due to tears or the formation of a sticky discharge.
  • Flu-like symptoms, such as general malaise, sore throat, muscle aches, and fever.

Conjunctivitis is typically diagnosed through a comprehensive eye examination performed by an ophthalmologist. The steps involved in diagnosing conjunctivitis include:

  • Collection of medical history to rule out conjunctivitis (the ophthalmologist asks questions about symptoms, any close contact with other people with conjunctivitis, and possible contact with eye irritants).
  • Slit-lamp examination (to examine various parts of the eye, including the sclera, conjunctiva, iris, and cornea). 
  • Visual acuity tests to ascertain whether conjunctivitis has affected the vision.

Eye culture (sampling of the cells from underneath the eyelids with a cotton swab for further examination by a pathologist to ascertain the causative pathogen).

Bacterial and viral conjunctivitis are highly contagious. They spread very easily via droplets (coughing or sneezing) or contact with fomites, such as tissues, towels, or pillowcases. To avoid the spread of infection, it is important to:  

  • Wash hands frequently.
  • Cover mouth while coughing or sneezing.
  • Dispose of tissues after use.
  • Avoid sharing contagious belongings. 

The following measures may be used to prevent allergic and other forms of non-contagious conjunctivitis: 

  • Allergy testing to identify potential triggers. 
  • Wash your face after being exposed to allergens like dust or pollen.
  • Keep windows closed during seasons when pollen or fungal spores are abundant. 
  • Wash your hands after petting animals.
  • Frequently cleaning the house.
  • Washing bedding/pillows using detergents and hot water.
  • Careful use of medications, cosmetics, and apparatus along with regular consultation with the physician.
  • Monitoring exposure to different activities (such as swimming) and environments (such as polluted areas). 

Most cases of infective conjunctivitis require no treatment as the infections are self-limiting and will clear up on their own within a few days to a few weeks. However, if the condition persists, treatment options for infective conjunctivitis include:

  • Antibiotic ointments or eye drops: These may be helpful in managing bacterial conjunctivitis. However, viral infections do not respond to antibiotics and may last for two to three weeks until the natural immunity of the host eliminates the virus.
  • Lubricating ointments, eye drops, or gels: These may help reduce discomfort and grittiness but not the duration of the illness.
  • Over-the-counter and prescription painkillers, such as paracetamol or ibuprofen (provided no medical reason prevents their use) can help alleviate the discomfort and flu-like symptoms associated with conjunctivitis.
  • Warm-water washes: This can be performed routinely to clean the sticky discharge from the eyes.
  • Steroidal eye drops: These are used to reduce inflammation in severe cases.

Treatment options include:

  • Avoiding rubbing of the eyes as it worsens symptoms.
  • Cold compress to help reduce eyelid swelling.
  • Application of lubricating ointments or eye drops may help reduce discomfort but will not treat the allergy.
  • Over-the-counter anti-allergy drops need to be used daily. These may require up to two weeks to work. While some people need to use these drops for only a few weeks in the summer, others may have to do so throughout the spring and summer months. However, depending on the severity of symptoms, some patients may also need to use these drop throughout the year.
  • Antihistamine tablets.
  • Steroid eye drops (used in severe cases).

Occasionally, viral conjunctivitis can cause keratitis (corneal inflammation) or conjunctival scarring, both of which can affect vision. However, these complications are usually manageable with treatment.

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C

Central Serous Chorioretinopathy (CSCR)

Management Team

Central Serous Chorioretinopathy (CSCR)

Overview

Central serous chorioretinopathy (CSCR), a common ophthalmic disorder, affects the macula, which is crucial for sharp, clear central vision. In CSCR, fluid accumulation below the macula causes the temporary distortion and blurring of vision. CSCR is common in people aged 20–50 years. Its incidence in men is higher than that in women.

No exact cause of CSCR has been identified. However, several risk factors for this condition have been identified:

  • Psychological stress, including traumatic life events or work-related stress.
  • Excessive or prolonged corticosteroid use (oral, inhalational, or topical administration).
  • The risk of developing CSCR may be particularly high in individuals with a Type A personality (who are highly competitive, ambitious, and driven and exposed to high levels of psychological stress).

The severity and duration of the symptoms of CSCR vary. These symptoms include:

  • Blurring or distortion of central vision in one eye (the most common symptom).
  • Appearance of dark spots in the central field of vision.
  • Heightened contrast sensitivity.
  • Decreased colour perception.
  • Objects appearing smaller than they are (micropsia).

To diagnose CSCR, an ophthalmologist will perform a comprehensive eye examination, which includes:

  • Retinal examination. The doctor dilates the pupils with special eye drops to examine the retina using a slit-lamp or ophthalmoscope for identifying cataracts and assessing any damage to the retina.
  • Visual acuity tests.
  • Collection of comprehensive medical history.
  • Accessory diagnostic tests, such as the estimation of choroidal thickness using enhanced depth imaging optical coherence tomography (OCT), OCT angiography (a non-invasive technique used to visualise the vasculature of the retina and choroidal layers), fluorescein angiography (injection of fluorescein into a vein to detect blood vessels in the eyes), and indocyanine green angiography (an invasive technique used to visualise the vasculature of the retina and choroidal layers). These tests help assess the degree of retinal involvement and confirm fluid leakage in the retina.

CSCR often resolves spontaneously even without specific treatments over a period of few months. However, various treatment options are available for patients showing persistent symptoms or those facing a high risk of complications:

  • Routine eye checkups and observations: As mild or early-stage CSCR is self-limiting, only regular monitoring may be required.
  • Lifestyle modifications: Adopting healthy lifestyles, reducing stress levels, and ensuring mental well-being can help prevent and treat CSCR.
  • Photodynamic therapy (PDT): This may be recommended to seal leaks in the choroidal blood vessels for patients with advanced CSCR and can help mitigate fluid accumulation in the retina.
  • Micro-pulse and low-power laser therapies. These are also useful in sealing leaks in the retina, promoting fluid absorption.
  • Anti-vascular endothelial growth factor (VEGF) agents: Intravitreal injections of specific therapeutics, such as anti-VEGF drugs, can help treat CSCR. These agents suppress abnormal angiogenesis (formation of new blood vessels) below the retinal layers.

Although CSCR causes discomfort and temporarily impairs vision, early diagnosis and the timely administration of appropriate treatments can ensure a complete recovery.

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C

Age-related Macular Degeneration (AMD)

Management Team

Age-related Macular Degeneration (AMD)

Overview

Age-related macular degeneration (AMD) refers to the ageing-induced damage of the macula, which is the central part of the retina. The macula, which consists of light-sensing tissues that line the back of the eye, is responsible for sharp, clear central vision. In AMD, the central vision is blurred, while the peripheral (side) vision is not affected. This common condition is the most prominent cause of vision impairment in people aged > 50 years.

The visual precision required for daily activities is greatly impaired by AMD. The progression of this disease interferes with several activities, including facial recognition, driving, and viewing details up close (for example, telling the time) or from afar (for example, trying to view a bus number), or reading.

Early diagnosis and timely treatment can impede the progression of AMD. Regular eye checkups, knowledge regarding risk factors, and prompt medical attention to alterations in vision are crucial for the preservation of eyesight. With proper eyecare and management, vision can be effectively maintained in patients with AMD.

  • Dry AMD: About 75%–80% of AMD cases represent the dry form. Genetic and environmental factors are thought to cause dry AMD although an exact cause has not yet been identified. Dry AMD involves the gradual degradation of the light-sensitive cells in the macula (generally, one eye at a time). The loss of vision is usually slow and gradual. Most patients experience near-normal vision or only slight vision loss. The ageing-induced deterioration of an important support membrane under the retina has been theorised to cause dry AMD.
  • Wet AMD: Although wet AMD is a less common type of AMD, it is the most common cause of severe loss of vision. Usually, vision loss after wet AMD is more severe than that after dry AMD. The occurrence of wet AMD occurs is attributed to the growth of abnormal blood vessels beneath the retina. This causes a leakage of fluid and blood (giving rise to the term ‘wet AMD’), which prevents the light-sensitive cells in the retina from functioning properly. Ultimately, due to the bleeding and scarring, a large blind spot is created in the centre of the visual field. This causes the permanent loss of central vision. However, as the peripheral (side) vision is not affected, complete vision loss is unlikely. Regular eye exams are recommended to diagnose wet AMD as it progresses more rapidly than dry AMD, preventing extensive vision loss. Geographic atrophy, a less common form of wet AMD, represents a condition involving the severe thinning or loss of the macula. However, there is an absence of leaking blood vessels. Antiangiogenic medicines are not effective against geographic atrophy.

The exact causes of AMD are unknown. However, certain patient groups have been reported to be at a higher risk of developing this condition. Such groups include subjects who are smokers and/or overweight and subjects with hypertension. A family history of AMD may also be a risk factor.

It is diagnosed by an ophthalmologist and confirmed with the help of additional imaging tests, such as:

  • Retinal scan to evaluate AMD severity.
  • Optical coherence tomography (OCT) of the macula. In this non-invasive imaging test, light waves are used to capture cross-section pictures of the retina.

Regular comprehensive eye exams, even in the absence of changes in vision, are advised for the early detection of AMD before major vision loss. Early detection and timely treatment are crucial to counter the impairment of vision caused by AMD progression.

Preventive measures for AMD include:

  • Cessation of smoking, consuming a well-balanced diet (to maintain a healthy weight), and following a healthy lifestyle, including regular exercise regimens.
  • Certain antioxidant-based and zinc-based supplements may halt the progression of AMD although their benefits have not been proven.

Treatment options for AMD include:

  • Wet AMD: Wet AMD is treated by injecting anti-vascular endothelial growth factor (VEGF) drugs, also known as anti-angiogenic medicines, into the eye. They prevent the growth and leakage of abnormal blood vessels and bleeding under the retina. In most cases, repeated injections are required several times per year to control wet AMD.
  • Dry AMD: No treatment options are currently available for dry AMD.
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A

Mitochondrial Disorders

Management Team

Mitochondrial Disorders

Overview

Mitochondrial neurological disorders are a group of conditions that affect the brain and nervous system due to dysfunction of the mitochondria, the energy-producing structures within cells. They may affect brain, spinal cord, nerves, or muscles and produce a cluster of symptoms. Mitochondrial neurological disorders can be caused by mutations in either mitochondrial DNA (mtDNA) or nuclear DNA (nDNA) and may be inherited in various patterns.

  • Mitochondrial myopathies (muscle disorders)
  • Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
  • Kearns-Sayre syndrome (KSS)
  • Leigh syndrome
  • Progressive external ophthalmoplegia (PEO)
  • Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE)
  • Mitochondrial DNA depletion syndrome
  • Friedreich's ataxia
  • Hereditary spastic paraplegia
  • Mitochondrial optic neuropathies (e.g., Leber hereditary optic neuropathy)

Caused by genetic mutations

  • Genetic mutations in mitochondrial DNA (mtDNA) or nuclear DNA (nDNA); however, many cases occur without a family history
  • Environmental toxins
  • Infections
  • Aging can negatively affect mitochondrial function and increase the risk of secondary mitochondrial dysfunction (SMD)

  • Muscle weakness and paralysis
  • Seizures and epilepsy
  • Cognitive impairment and dementia
  • Vision loss and blindness
  • Hearing loss and deafness
  • Ataxia (coordination and balance problems)
  • Spasticity and stiffness
  • Peripheral neuropathy

Neurologist

  • Clinical evaluation
  • MRI brain
  • Muscle biopsy in mitochondrial myopathy
  • Genetic testing

  • Supportive care- Rehabilitation
  • Genetic counselling
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M

Cataract

Management Team

Cataract

Overview

A cataract refers to the clouding of the lens inside the eye, which ultimately becomes opaque and results in the gradual blurring of vision. The lens of a normal eye is clear, which helps focus light rays onto the retina (back of the eye) and the transmission of visual signals to the brain, enabling us to see. During cataract development, the clouding of the lens prevents the light rays from being focussed onto the retina. Thus, the picture received by the retina is dull and blurry.

Most forms of cataracts develop in adult life. Ageing causes the lens to become cloudy and harden. This represents the most common type of cataract and is referred to as an age-related cataract. Cataracts usually occur in patients aged > 40 years. However, other age-independent types include congenital (present at birth), traumatic (injury to the eye), and drug (steroids)-induced cataracts. Furthermore, the risk of cataract development among individuals with certain pre-existing conditions, such as diabetes, is higher than that among healthy individuals.

Cataracts, which usually form slowly over a few years, cause gradual vision blurring. Thus, corrective glasses are not sufficient for visual correction. In some cases, the deterioration of vision is rapid. Cataracts may also cause glares and the formation of multiple images in the retina of the affected eye, markedly affecting visual acuity and complicating daily activities, such as reading, driving, and recognising faces.

Cataracts are diagnosed by ophthalmologists during routine eye examinations. To confirm the diagnosis, the following examinations can be performed:

  • Visual acuity test to indicate the sharpness of vision.
  • Slit-lamp examination to closely examine the structures at the front of the eye (cornea, iris, lens) and spot abnormalities in the lens that may indicate cataracts.
  • Retinal exam, where the doctor dilates the pupils with special eye drops to examine the retina using a slit-lamp or ophthalmoscope for identifying cataracts and assessing any damage to the retina.
  • Refraction and contrast sensitivity tests to measure how the cataract is affecting vision and to check for other refractive errors, such as myopia, hyperopia, or astigmatism.

Currently, automated eye surgery, one of the most prolific hallmarks of advanced eye care, represents the primary method for treating cataracts (to remove the cataract). During the cataract surgery, the natural lens, which has turned cloudy and opaque, is replaced with an intraocular lens (a clear, artificial lens). This is a safe, painless, and routine outpatient surgery. Cataract surgeries are performed on a day-care basis, where the admission, surgery, and discharge happen on the same day. Cataract surgeries are of the following two types:

  • Refractive surgery: This is the most common cataract treatment. It involves a refractive lens exchange operation to replace the cloudy lens with an intraocular lens. The procedure is quick, takes 20–30 minutes, and can greatly improve vision.
  • Laser cataract surgery: For this procedure, a femtosecond laser is used to partially break down the cataract. The subsequent procedure is similar to that of conventional (non-laser) cataract surgery. Currently available evidence shows that both conventional and laser cataract surgery are equivalent in terms of vision and safety.

In recent years, precision surgery, such as that using the Alcon Lens Laser (a cutting-edge technology used in ophthalmology for precise and automated cataract surgery), and advanced robotic surgery have also emerged as efficient surgical modalities for cataract removal. These advanced techniques are associated with high accuracy and rapid treatment and recovery, resulting in reduced levels of stress for patients, increased levels of comfort, and enhanced cataract surgery outcomes.

Cataract surgery recovery durations differ for every person. Usually, outpatient recovery is possible. Most patients recover quickly within approximately 3–4 days. During recovery, it is normal for vision to take a few days to improve. The eyes may also be sore, scratchy, and light-sensitive. Antibiotic and anti-inflammatory drops are initiated the day after surgery. Patients can return to work a few days after surgery. However, if a job is physically demanding, recovery may require a longer duration. The treating physician determines the recovery duration.

Once the cloudy (cataractous) lens has been removed in surgery, it does not recur. However, after a few months or years after cataract surgery, the thin membrane behind the new lens implant (posterior capsule) may become opaque. This creates a “filter effect” and can cause the deterioration of vision. A simple laser treatment (YAG laser capsulotomy), which is usually an outpatient procedure, can be performed to clear this membrane and restore vision.

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C

Blepharitis

Management Team

Blepharitis

Overview

Blepharitis refers to the inflammation of the eyelids. This condition causes irritation and itchiness in the eyelids. Patients with blepharitis often exhibit greasy and crusted eyelids with scales sticking to the eyelashes. Blepharitis commonly occurs as a result of the clogging of the Meibomian glands (tiny oil glands near the base of the eyelashes). Some patients with blepharitis wake up with their eyelids stuck together, while others may experience dried tears and/or the feeling of something being stuck in their eyes. Although blepharitis is a chronic difficult-to-treat condition and can cause discomfort, it does not permanently damage eyesight and is not contagious.

The exact cause of blepharitis is unclear. However, one or more of the following factors are usually associated with this condition:

  • Dry eyes.
  • Seborrheic dermatitis (eyebrow and scalp dandruff).
  • Other types of eye infections.
  • Meibomian gland clogging or dysfunction.
  • Rosacea (a skin condition characterised by facial redness).
  • Allergies, including those to eye makeup, contact lens solutions, or eye medications.
  • Lice or eyelash mites.

Typically, the symptoms of blepharitis are worse in the morning. Such symptoms include:

  • Red and/or watery eyes.
  • Red, itchy, and/or swollen eyelids.
  • Sticky eyelids that often appear greasy.
  • Crusted eyelashes.
  • Flaking of the skin around the eyes.
  • Burning, gritty, or stinging sensations (eye irritation).
  • Frequent blinking.
  • Heightened light sensitivity.
  • Blurred vision (usually improves with blinking).

Blepharitis is typically diagnosed through a comprehensive eye examination performed by an ophthalmologist. The steps involved in diagnosing blepharitis include:

  • Collection of medical history to assess the history of skin conditions (like rosacea or seborrheic dermatitis) or allergies.
  • Physical examination of the eyelids, eyelashes, and tear film. This includes looking for signs of inflammation, crusting at the base of the eyelashes, or abnormal oil gland function in the eyelids.
  • Slit-lamp (a specialised microscope) examination to magnify and light up the eyelid and eye surface for a detailed view of the eyelid margins, meibomian glands (which can become blocked), and the overall condition of the tear film.
  • Tear sample or swab (if necessary) to rule out bacterial or fungal infections or to check for demodex mites (which cause blepharitis).

In most cases, self-care measures, such as regular eye washes and the use of warm compresses, are adequate for treating blepharitis. If these measures do not help, certain medications may be prescribed:

  • Infection-targeting medications: Antibiotics are useful in alleviating the symptoms and treating bacterial infections in the eyelids. These are available as eyedrops, creams, and ointments. Oral antibiotics may be prescribed if no response is observed with topical antibiotics.
  • Anti-inflammatory medications: Steroid-based eyedrops or ointments are used for patients who do not respond to other treatments. These may be prescribed together with antibiotics.
  • Immunomodulatory medications: Topical cyclosporine (Restasis) has been reported to ameliorate some symptoms of blepharitis.
  • Medications for treating underlying conditions: In cases where blepharitis is caused by conditions, such as rosacea, seborrheic dermatitis, or other diseases, treating the underlying disease may help alleviate the signs and symptoms of blepharitis.
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B

Migraine

Management Team

Migraine

Overview

Migraine is a neurological disorder causing hemicranial headache and affecting the quality of life of patient.

  • Exact cause is unknown
  • Genetic
  • Stress
  • Hormonal changes
  • Medications
  • Sleep disorders
  • Weather changes
  • Overexercise
  • Caffeine or tobacco
  • Skipping meals
  • Bright lights, loud sounds, or strong odours

  • Family history
  • Female sex
  • Migraines usually begin during adolescence and peak in 30s.
  • Hormonal changes
  • Other medical conditions including depression, anxiety, bipolar disorder, sleep disorders, and epilepsy
  • Medications

  • Throbbing pain in one half of the head, starting in forehead and radiating backwards
  • Nausea and vomiting
  • Sensitivity to light and sound
  • Headache preceded by fatigue or low mood
  • May or may not be associated with aura- visual phenomenon with scintillating lights appreciated in visual field
  • Headache increases in intensity gradually, may remain for 48–72 hours.
  • Precipitated by lack of sleep, hunger, stress, exposure to heat or cold, certain smells or food items
  • Frequency and intensity vary from person to person

Neurologist

  • Clinical examination
  • MRI brain if any red flags in the history or papilloedema

Based on examination, migraines can be classified as follows:

  • Migraine with aura
  • Migraine without aura
  • Abdominal migraine
  • Basilar migraine
  • Silent migraine
  • Chronic migraine
  • Status migrainosus

  • Abortive medications like paracetamol and others
  • Prophylactic medications to decrease headache frequency
  • Medications available as subcutaneous injections in refractory and chronic cases
  • Botulinum injection in refractory cases
  • Transcranial magnetic stimulation is also done in refractory cases
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