Brainstem Auditory-evoked Response (BAER) Brainstem Auditory-evoked Response (BAER) Home Overview The brainstem auditory evoked response is a non-invasive test used to assess the function of auditory nerve and brainstem. It measures the electrical activity generated in response to an auditory stimulus. Method Electrodes are placed on the scalp and earsPatient listens to sounds generated in the form of clicks and tonesThe brain activity generated in response to the sound is recorded Indications New-born screening for hearing disordersDiagnosing auditory nerve damageMonitoring brain stem function in comatose patientsDiagnosing hearing loss or deafnessDiagnostic tools in acoustic neuroma or multiple sclerosis Read more about Brainstem Auditory-evoked Response (BAER) Filter Alphabet B
Periodic Paralysis Periodic Paralysis Home Overview Periodic paralysis is a group of disorders with episodic muscle weakness. The dysfunction of ion channels interferes with muscle depolarization and in turn causes muscle weakness. Correction of these electrolytes causes rapid correction of muscle weakness. Causes Caused due to dysfunction of ion channels leading to hypo or hyperkalaemia. Hypokalaemia periodic paralysis This shows autosomal dominant inheritance and is caused by CACNA1/ SCNA gene mutation Symptoms Recurrent paralysis lasting hours to daysLow potassium levelsMuscle cramps/ spasmsPrecipitated by high carbohydrate diet, stress, and alcohol consumption among othersSymptoms vary in severity and frequency Hyperkalaemia periodic paralysis It is similar to hypokalaemia periodic paralysis, except that it gets precipitated by raised potassium levels (hyperkalaemia) and is treated by potassium lowering agents such as diuretics. Risk factors Risk factors for periodic paralysis include:Abnormal Potassium levelsAge of onset: the first paralytic attack usually occurs between the ages of two and 30,Female sexIndividuals of Asian or Hispanic descentAbnormal thyroid hormone levelsCertain medicationsEating potassium-rich foods, high-carbohydrate meals, or skipping mealsResting after exercise can trigger attacks.StressPregnancyExposure to extreme temperatureViral illness Diagnosis Low potassium levelsECG changes due to hypokalaemiaNCV may show axonal neuropathyGenetic testing Specialist to approach Neurologist Treatment Correction of potassium levelsPhysiotherapyMuscle strengthening on a regular basisDietary and lifestyle regulation Read more about Periodic Paralysis Filter Alphabet P
Myoclonus Myoclonus Home Overview Myoclonus is a sudden shock-like involuntary movement, which can be sudden contraction of muscle (positive myoclonus) or a pause in muscle activity (negative myoclonus or asterixis). The following types of myoclonuses have been determined:Based on distributionGeneralizedFocalMultifocalSegmentalBased on clinical presentationSpontaneousActionReflex (auditory, visual, or to touch)Based on site of origin:Cortical myoclonus- myoclonic jerks triggered by movement or stimulus-sensitive. EEG may be diagnostic: cortical discharges time-locked to myoclonic jerks; giant cortical somatosensory evoked potentialsBrainstem myoclonus- bilateral synchronous jerking with adduction of arms, flexion of elbows, flexion of trunk and head. Stimulus-induced: tap nose, lip, or head or loud noiseSpinal cord- rhythmic, repetitive, bilateral, jerking one or two adjacent parts Causes Physiological- hypnic jerks and hiccupEpilepsy- focal epilepsy (Epilepsia partialis continua), myoclonic epilepsies-progressive myoclonic epilepsy (Unverricht–Lundborg disease)Encephalopathy: metabolic (liver, renal failure)Infections: prion diseases, HIV, SSPEPost-anoxicDrugs: tricyclics, L-dopaDegenerative conditions: Alzheimer’s disease, MSA, corticobasal degeneration, celiac diseaseHereditary: HD, mitochondrial disorders, myoclonic dystonia (DYT 11), storage disordersFocal lesions brain or spinal cord Risk factors Nervous system disorders such as multiple sclerosis, epilepsy, Parkinson's disease, Alzheimer's disease, or Creutzfeldt-Jakob diseaseBrain or spinal cord injuries, brain tumours, or strokesInfections such as meningitis or encephalitisProlonged oxygen deprivation to the brain (hypoxia)Family historyCertain medications like anticonvulsantsOther conditions such as kidney or liver failure, chemical or drug intoxication, metabolic disorders, or autoimmune inflammatory conditions Specialist to approach Neurologist Treatment Medical treatment is initiated per clinician’s evaluation and underlying cause Read more about Myoclonus Filter Alphabet M
Bone Marrow Bone Marrow Home Overview The bone marrow is the factory where all your blood is made. It produces: Platelets that stop you from bleeding when you get a cut or fall over and hurt yourself.White blood cells that help your body to fight infections.Red blood cells that give you energy to help you run around and play. Tests Before your child’s transplant, they will undergo several tests to ensure they are ready for the procedure. These may include:X‑rayUltrasound ScanBlood TestsBreathing TestsHeightKidney TestWeightAny other test as per doctor discretion Treatment To prepare for the transplant, your child will need a central line inserted, which will stay in place for several months. This line is used for administering blood tests, treatments, and medications. While it won't interfere with your child’s daily activities like attending school, swimming will be restricted.Your child will receive preparatory treatment before the transplant. This treatment can range from a few days to two weeks and may include chemotherapy, radiotherapy, or both.Chemotherapy involves special medications that are either administered through the central line or taken orally to target and destroy any malfunctioning cells in the body, including the bone marrow cells, to make way for the new, healthy bone marrow cells.Radiotherapy is not given to all children who have a bone marrow transplant. Radiotherapy is a special kind of X‑ray whose job it is to kill any cells in your body that don't work properly and to destroy your bone marrow. Having radiotherapy does not hurt. It is very important that your child keeps still for his / her radiotherapy which will last about 20 minutes. No one else can stay in the room with your child while he / she has his / her radiotherapy but they can usually see and hear you on a special television screen.The need for chemotherapy and radiotherapy will be decided by your doctor and will be discussed with you in detail.Chemotherapy and radiotherapy can cause temporary hair loss about 2 weeks later, including eyebrows and eyelashes. Many children choose to have their hair cut short before treatment or wear a wig, cap, or hat until their hair grows back, which typically takes 3-6 months. Sometimes hair can be a bit darker or a bit lighter when it grows back. How to look after your child's mouth? Chemotherapy and radiotherapy can make your child's mouth sore and may cause nausea. To help manage this:Encourage your child to drink small sips of water or suck on ice cubes.Maintain good oral hygiene. We would like your child to clean your teeth 3‑4 times a day with a soft toothbrush and toothpaste. If mouth sores make brushing difficult, special sponges can be used instead.Inform the nurses if your child feels sick or has mouth pain so they can provide the necessary treatments to ease discomfort. Ryle's / Feeding Tube If your child has trouble eating, they may require a feeding tube to get the nutrition they need. The tube could also be used for medicines which can really help your child. If the feeds make your child too sick, special feeds (TPN) may be administered through a Hickman line. A feeding tube is essential during recovery to keep your child strong. At Home During the recovery phase, your child’s bone marrow will be destroyed, leading to a lower white blood cell count and a weakened immune system. To protect against infections:Your child will stay in a private room, rather than sharing with other children, to minimize exposure to germs. A family member will be able to stay with your child to help with care.Daily Seitz baths (sitting in a tub for 15-20 minutes) are recommended for hygiene and comfort.Your child's hair will start growing back after a few months. Diet and Nutrition Certain foods may not be allowed during the transplant period, as they could cause digestive upset. Your child will probably not be able to eat the skin on fruit, a half boiled egg, etc. A list of recommended foods will be provided by the hospital’s dietitians, and the nurse will guide you on which foods are safe for your child. Feeling Better and Visiting As your child’s new bone marrow begins to function, they will gradually be able to interact more and leave their room. The doctors and nurses will monitor blood counts to determine when it is safe for your child to have visitors or leave their room. If an infection is present, your child may need to stay in isolation for longer. Medicines At home, your child will need to continue taking medications. You may be able to choose between liquid or tablet forms. Please ask if the options aren’t provided. Follow-Up Visits After leaving the hospital, your child will have regular check-ups to monitor recovery and prevent complications. Your child may need to stay on special medications if they experience side effects such as rashes or digestive issues. Sometimes you may have to come back into hospital for a few days in case of any problem. Returning Home Once your child leaves the hospital, it’s important to limit exposure to germs:Keep visits to a few close friends who are healthy and free of infections.Avoid crowded places like shopping malls for the time being.Short walks outside in fresh air are encouraged if your child feels strong enough.School attendance may be delayed for a few months. Initially, your child may return for half-days or a few hours at a time.Your child will likely feel tired, especially if they have undergone radiotherapy. This is normal, and with time, their energy levels will improve. Line Once your child no longer needs the central line for blood tests or treatments (usually around 3-6 months after the transplant), it will be removed. At that point, your child can resume swimming and enjoy regular baths. Read more about Bone Marrow Filter Alphabet B
Myasthenia Gravis (MG) Myasthenia Gravis (MG) Home Overview MG is a neuromuscular disorder, whose prevalence peaks at 20–30 years or 60–70 years of age. MG is characterized by fatiguability, where initial part of movement can be done smoothly and then the power decreases on continued activity. Causes Generation of autoantibodies against acetylcholine receptors at the neuromuscular junction and MuSK, LRP, ryanodine, and titin proteins. This leads to failure of conduction of action potential from nerve to muscle, leading to weakness.Thymus is abnormal in 75% of patients: hyperplasia (85%) and thymoma (15%)Other autoimmune conditions associated with MG are thyroiditis, Graves’s disease, rheumatoid arthritis, systemic lupus erythematosus, pernicious anaemia, Addison’s disease, and vitiligo. Risk factors Certain genetic markers, such as HLA-B8 and DR3Autoimmune disorders such as lupus, rheumatoid arthritis, or thyroid diseaseInfants of mothers with myasthenia gravis may develop neonatal myasthenia gravisSmokingMedications including antimalarials, certain antibiotics, and medications used to treat heart rhythm irregularities Symptoms Painless muscle weakness following exerciseIn 15–20% cases, only the ocular muscles are involved, whereas in 85% of the cases, the weakness is generalizedOther presenting features include dysphagia (6%), dysarthria and dysphonia (5%), jaw weakness (4%), and neck weakness (1%).Rarely, respiratory failure and isolated foot drop may be presentedExacerbation of weakness by drugs (aminoglycosides, quinine, anti-arrhythmic drugs) Specialist to approach Neurologist Diagnosis Clinical suspicion should guide further investigationsAntibody panel- Anti acetylcholine receptor antibody, anti-Musk antibody, anti LRP antibodiesRepetitive nerve stimulation- sensitive in 50–60% of cases (see chapter 6)Single fibre EMG studies- detect delay or failed neurotransmission in pairs of muscle fibres supplied by a single nerve fibreTensilon (edrophonium) test- uses a rapid onset (30 seconds) short-acting (5 minutes) cholinesterase inhibitor drug. An unequivocal improvement in a muscle is considered a positive resultPost-contrast CT or MRI of the mediastinum to check for thymomaOther tests such as thyroid function and thyroid antibodies test among others may be needed Treatment Cholinesterase inhibitorsImmunomodulatorsSupportive treatment with calcium, bisphosphonates, vitamin D, and antacidsImmunosuppressants may be used as steroid sparing agentsBlood tests (FBC and LFT) necessary every week for 2 months and then 3 monthly for the duration of treatment to monitor immunosuppressionPlasma exchange and IV immunoglobulin given in cases of sudden deterioration with impending respiratory failure, dysphagia, severe worsening of weakness for immediate relief of symptoms (myasthenia crisis)Thymectomy when thymoma is found in CT chest to eliminate the source of abnormal antibodies. Read more about Myasthenia Gravis (MG) Filter Alphabet M
Retinal Detachment Retinal Detachment Home Overview Retinal detachment refers to the separation of the delicate layer of receptors at the retina from the oxygen-supplying blood vessels. As the detachment of the retina may lead to permanent vision loss if left untreated for a long duration, immediate medical attention and emergency surgery are advised.The retina, which contains many layers of interconnected photoreceptor and glial cells that line the inside of the eye, is sensitive to light (like a camera film) and is thus crucial for proper vision.One or more holes in a retina could cause it to detach. Fluid tends to pass via these holes and is accumulated. This causes the retina to separate from the supporting tissues underneath it. Furthermore, small blood vessels may also leak blood into the vitreous humour, further clouding the vision. If left untreated, retinal detachment often leads to permanent blindness. Causes In most cases, retinal detachments are associated with the normal ageing process. This is referred to as posterior vitreous detachment (PVD), which cannot be prevented. Although a retinal detachment could happen to anyone, certain factors increase the risk of developing this condition. These risk factors include:Short-sightedness.Previous cataract surgery.Severe direct trauma to the eye.In some cases, retinal detachments may be hereditary, which is rare. Symptoms Although retinal detachment is painless, several visual symptoms appear before it advances. These signs include: Appearance of floaters (shapes or spots (visible as small dots or irregular strands, among others) drifting across the visual field).Appearance of flashes of light in one or both eyes.Blurring of vision.Appearance of a curtain-like shadow encompassing the field of vision.Gradual loss of peripheral vision.If any of the above symptoms are noted, patients are advised to seek medical attention immediately or within a maximum of 48 hours. This will help rule out a retinal tear or detachment and minimise the long-term visual damage that the retinal detachment may cause. Diagnosis Eye surgeons usually perform associated tests to confirm a retinal detachment or tear. Once this confirmation is obtained, the patient is referred to the hospital to undergo laser surgery or other surgical procedures to reattach the displaced retina. Treatment Retinal surgery to reattach the retina to the back of the eye and sealing any breaks or holes in the retina can prevent blindness. The sight has already been lost because of the detached retina. If the surgery is successful, it will usually bring back some but not all lost eyesight.Preoperative preparationAs most surgical procedures to correct retinal detachment are performed after the administration of a local anaesthetic, the patient is awake throughout the operation. The local anaesthetic is injected into the area surrounding the eye to numb it and prevent any pain during the surgical procedure.ProceduresOne of the following procedures is used to repair retinal detachment:Cryopexy and scleral buckle: the retinal holes are sealed by placing ‘splints’ (buckles made of sponge or solid silicone material) along the wall of the eye. These buckles are positioned outside the sclera (the white of the eyeball) (under the skin of the eye). They remain fixed there permanently.Vitrectomy, cryopexy, and gas, air, or silicone oil injection: For vitrectomy operations, which are referred to as keyhole surgeries for the eye, tiny openings (less than 1 mm in size) are created in the eye by the surgeon, who then removes the vitreous humour. Next, the surgeon locates the retinal breaks and subjects them to treatment with laser or cryopexy (freezing), which causes adhesion and scarring that seals the breaks. Seal formation usually requires up to 10 days. Next, a gas bubble, air, or silicone oil (used as tamponades) is inserted into the eye to function as ‘splints’, holding the retina in place until the tears are sealed. This process is termed as “intraocular tamponade.” “Tamponade” (the use of a tampon) refers to the insertion of a plug tightly into an orifice or a wound to prevent haemorrhage. In ophthalmic medicine, tamponade agents, which provide surface tension across retinal breaks, enable surgeons to prevent further fluid leakage into the subretinal space until the leak can be permanently sealed (using cryopexy). The three types of gases used for intraocular tamponade include:C3F8 (octafluoropropane) is a long-acting, non-flammable, non-toxic, synthetic gas and can remain in the eye for up to 12 weeksSF6 (sulphur hexafluoride) is a highly stable gas and can remain in the eye for up to 4 weeksC2F6 (hexafluoroethane) is a non-flammable, inert gas and can remain in the eye for up to 8 weeksPostoperative careEye drops: They reduce inflammation (anti-inflammatory eyedrops) and prevent infection (antibiotic-based eyedrops).Avoiding rubbing the eye: This may increase the chances of infection and complications.Analgesics (such as paracetamol): This relieves pain or discomfort.It is important to note that:Itchy and/or sticky eyelids and mild discomfort (gritty sensation caused by the stitches) are normal for 5–10 days after surgery.Some fluid leakage from around the eye is a common observation after surgery.Blurred vision after surgery is normal.In some cases, especially after a scleral buckle procedure, the area surrounding the eyes may show slight bruising.Rest is important for healing.Any discomfort should ease after 1–2 days. The eye requires about 2–6 weeks to heal in most cases. An appointment with the treating doctor is usually scheduled within 7–14 days of surgery.If the pain or blurry vision intensifies after the operation, the patient is advised to contact the hospital immediately as further treatments may be necessary. Recovery Usually, retinal detachment surgeries are outpatient procedures. Thus, overnight hospital stays are not needed and recovery can take place at home.Working and driving should be avoided during recovery. If a gas bubble was inserted into the eye during surgery, flying should be avoided for a certain period of time. This is because the pressurised environment in airplanes may cause the gas or air bubble to expand in size, increasing intraocular pressure and causing vision loss.Posturing is the hardest, but the most crucial, part of recovery. If a gas bubble or silicone oil is inserted into the eye, the patient is asked to ‘posture’ for up to 7 days, i.e., lying or sitting to position the head in a manner that enables the bubble to float up and press the retina into position during the healing process. The surgeon will determine the necessity and appropriate position for posturing. With the dispersion of the gas bubble, a moving line will begin to appear in the field of vision. The vision above the line is clear, but that under the line will be blurry or fuzzy. Eventually, the gas will disperse until it gradually disappears. The type of gas used determines the duration for which it will stay in the eye. Outcomes Recovery of vision usually requires a few weeks after surgery. The insertion of a gas bubble will cause the vision to be very blurry immediately after surgery. However, this is normal; once the retina is attached, the vision will improve gradually over a period of several months.Visual acuity tests are performed to ascertain whether glasses are needed to improve vision. The final quality of vision depends on the severity and nature of the original retinal detachment. With timely diagnosis and treatment, most of the central vision can successfully be restored. However, if the central vision is already poor during the diagnosis of a retinal detachment, restoring the central vision in its entirety may not be possible. Reading using the affected eye may be difficult. From a distance, faces or car number plates may be difficult to recognise. However, objects and people approaching from the sides may be visible; this is important, given that peripheral vision is critical for daily activities, such as climbing stairs and going out. Complications Given that each patient is different and that some cases of retinal detachment are more complicated to treat than others, retinal detachment surgeries are not always successful; further, in some instances, more than one operation may be required.After a retinal detachment, the eye tries to heal this damage naturally. However, this healing process is counterproductive, as it leads to the formation of scar tissue inside the eye and causes the retina to contract. This is referred to as proliferative vitreoretinopathy (PVR), a condition associated with poor vision that can cause the retina to detach once again (after it was surgically reattached). Around 5–10% of patients display scar tissue formation or develop another retinal tear, both of which will require additional surgeries. Read more about Retinal Detachment Filter Alphabet R
Uveitis Uveitis Home Overview Uveitis refers to inflammation of the uvea (the middle layer of the eye). The uvea comprises the iris (the coloured part of the eye), ciliary body (a thin, ring-shaped membrane behind the iris), and choroid (a vascular tissue layer supporting the retina).While uveitis may be idiopathic (autoimmune or unknown causes) or arise as a consequence of an underlying systemic disease or infection, it can also result from an injury or in rare cases, from ocular surgery. If left untreated, uveitis can cause serious damage to the eye and severely affect eyesight.Uveitis has also been associated with further ocular complications, including glaucoma and cataract development. However, in most cases, patients recover well after treatment. Diagnosing uveitis early is critical as the timely diagnosis and treatment of this condition markedly improves the patient outcomes.Uveitis can affect anyone. However, uveitis most commonly affects people of working age, especially in the aged group of 20–59 years, and can occur in children.Based on the affected part of the eye, uveitis may be categorised as follows:Anterior uveitis: Inflammation of the iris (iritis) or the collective inflammation of the iris and the ciliary body (iridocyclitis). It affects the front of the eye (usually the iris). Depending on the cause, one or both eyes are affected. It is most common type, accounting for 75% of all uveitis cases in adults.Intermediate uveitis: The vitreous humour is affected. This occurs in children, teenagers, and young adults and is the second most common type of ocular inflammation.Posterior uveitis: A severe form of uveitis that affects the choroid and the retina (back layers of the eye). It can seriously damage visual acuity.Panuveitis: Affects the entire uveal tract (the simultaneous inflammation of the front and the back of the eye). This condition seriously threatens vision and requires immediate medical attention.Based on the duration for which it lasts, uveitis may also be categorised as follows:Acute uveitis: Lasts for 2–3 weeks and can recur.Chronic uveitis: Lasts for three or more months, with symptoms varying over the course of the disease.Repeated episodes of inflammation in the eye may also occur at intervals of a few months between each episode. This is termed as recurrent uveitis. Causes Uveitis is broadly categorised into the infectious and non-infectious types. Often, the exact cause of uveitis is unclear. After clinical investigation, no specific cause can be pinpointed for roughly 40% of patients. In many cases, uveitis is linked to an increased degree of immune responses in the eye (occurring due to unknown reasons). In rare cases, uveitis has been reported to be caused by injuries or infections or as a complication of surgical procedures.The following health conditions have been reported as risk factors for uveitis:Inflammatory or autoimmune conditions (when the body attacks its own organs), such as rheumatoid arthritis (autoimmune joint inflammation), ankylosing spondylitis (also known as lumbar (lower back) arthritis), inflammatory bowel disease, or psoriasis, or other systemic conditions, including sarcoidosis (formation of lumps (granulomas) in various body parts), Behçet’s disease (inflammation and damage of blood vessels), and Reiter’s disease (inflammatory arthritis triggered by bacterial infections).Bacterial (tuberculosis, Lyme disease, etc.), viral (herpes simplex virus infection, herpes zoster infection (shingles), etc.), fungal infections (candidiasis, aspergillosis, etc.), and parasitic infections (toxoplasmosis, filariasis, etc.). The development of immunodeficiency or an immunocompromised state, which are commonly observed in patients with known underlying conditions, such as lymphoma, leukaemia, and/or HIV/AIDS may increase the susceptibility of these patients to opportunistic eye infections, such as cytomegalovirus retinitis.Juvenile idiopathic arthritis (JIA). In children, JIA has been identified as the most common cause of uveitis. Symptoms The symptoms of uveitis may vary in intensity from mild to severe depending on the type of the disease.Anterior uveitis symptoms may progress over several hours or days. Their severity may gradually increase. They include:An aching, painful, red eye, ranging from mild eye pain to intense discomfortCloudy or blurry visionDecreased pupil size or distortion of pupil shapeSlight alterations in iris colourSensitivity to light (photophobia)HeadachesIntermediate uveitis is usually painless and affect both eyes. The symptoms of this condition include:Floaters (dots that move across the field of vision)Blurry vision due to the leakage of proteins and cells from the blood vessels into the vitreous humour because of retinal vasculitis (inflammation of retinal blood vessel walls) or pars planitis (the formation of deposits behind the ciliary body)Mild redness (despite the symptoms, the inflamed eye may appear completely normal)Posterior uveitis is usually painless and affects one or both eyes. Its symptoms develop slower, and often last longer, than those of anterior uveitis. This condition can cause a greater degree of ocular damage than other types of uveitis. Its symptoms include:Decreased vision and floatersRetinal detachmentIn some cases, loss of vision Diagnosis As uveitis is predominantly diagnosed based on clinical examinations, meticulous collection of patient history (ocular and systemic history) is vital. Further tests to confirm or exclude certain eye and/or systemic conditions may be recommended based on the symptoms, presentation, and severity of the condition. These include:Comprehensive eye examinations that include the collection and assessment of a complete, detailed medical history (overall ocular health and general health).Assessment of eye scans and/or photographs, especially using the slit-lamp examination.Blood tests to detect the causative pathogen (for cases of infectious uveitis).Chest radiography (X-ray) to identify any underlying condition that may be the cause of uveitis.Tests for rheumatoid arthritis (RA) factor, serum uric acid tests, the purified protein derivative (PPD) skin test or Mantoux test (skin tests for detecting tuberculosis in which a PPD is injected into the forearm, and the diameter of the resulting swelling is measured after 48–72 hours), tests for the levels of HLA B-27, acetylcholine esterase (ACE) inhibitors, and C-reactive protein, fluorescent treponemal antibody absorption (FTA-ABS) test, perinuclear anti-neutrophil cytoplasmic antibody (P-ANCA) and cytoplasmic ANCA (C-ANCA) level measurements, and serum IgG and serum IgM antibody tests are usually recommended in cases of suspected uveitis.Based on the results of the aforementioned analyses, ophthalmologists recommend further tests to be conducted. Treatment The type and underlying cause of uveitis usually determine the recommended course of action and treatment. However, an exact cause cannot always be identified. The methods used for treating uveitis include:Steroid medications, which are the most common uveitis treatment modality, help reduce inflammation. While steroid-based eyedrops are usually administered for treating anterior uveitis, steroid-based tablets or injections (administered as systemic medications) may be required for treating severe cases of anterior uveitis and several types of non-infectious posterior uveitis.Additional treatment, usually in the form of eye drops, may be prescribed for pain relief or dilation of the pupils.In rare instances, such as uveitis cases in which cataract or glaucoma development is observed (eye drops are unable to mitigate the increase in intraocular pressure), surgery may be needed. Complications In most cases, patients with uveitis, especially, those with anterior uveitis, respond quickly to treatment without any long-lasting eye damage or further complications. However, the risk of complications is markedly high among patients with intermediate or posterior uveitis or those with recurrent uveitis. These complications include retinal damage, glaucoma, cataract development, macular oedema, and the permanent deterioration of vision. Read more about Uveitis Filter Alphabet U
Multisystem Atrophy (MSA) Multisystem Atrophy (MSA) Home Overview Multisystem atrophy is a progressive neurodegenerative disease, which affects the autonomic system and the motor system. Causes MSA is caused due to deposition of abnormal synuclein protein (synucleinopathy) in the brain. Risk factors Genetic variations in certain genes including SNCA and LRRK2Age group: 50-60 yearsMale sexHistory of neurological conditions such as Parkinson's diseaseVascular risk factors including hypertension, diabetes mellitus, hyperlipidaemia,Exposure to solvents, certain types of plastic or metal, and other potential toxinsRapid eye movement (REM) sleep behaviour disorderAutonomic nervous system conditions Symptoms Autonomic disturbances such as postural hypotension and urinary incontinenceParkinsonian signs such as bradykinesia and rigidityCerebellar signs such as ataxia and inability to coordinatePyramidal signs such as weakness and spasticityMyoclonic jerksSleep disorders such as sleep apnoea, REM behavioural disorders, excessive daytime sleepiness, and nocturnal sleep disturbancesRespiratory complications such as stridorDysphagia at later stagesCognitive disability in later stages Specialist to approach Neurologist Diagnosis Clinical history and examinationMRI Brain to determine hot cross bun sign in brain stem.Polysomnography to check for sleep disordersAutonomic nervous testing Treatment No specific treatment is available.Supportive care for prevention of orthostatic hypotension, sleep disorders, dysphagia, stridor, and parkinsonian symptoms Read more about Multisystem Atrophy (MSA) Filter Alphabet M
Glaucoma Glaucoma Home Overview Glaucoma comprises a group of eye conditions associated with damage to the optic nerve (the nerve that connects the eye to the brain) to the point where it detaches from the eye. It is one of the leading causes of vision loss globally. In the UK, approximately 2% of people aged > 40 years are reported to have glaucoma.While any vision loss resulting from glaucoma cannot be recovered, early diagnosis, routine monitoring, and accurate treatment strategies can greatly help suppress further loss of vision and preserve eyesight long-term in most patients. Glaucoma is usually difficult to detect as there are no warning sign. Routine eye examinations will help ascertain the onset and progression of this condition.Glaucoma may be categorised into the following four types:Primary open angle glaucoma, which develops very slowly, is the most common type of glaucoma. The risk of developing this condition is high among Black African or Black Caribbean populations.Angle closure glaucoma may develop slowly (chronic) or rapidly (acute) with a sudden, painful elevation of intraocular pressure. Asian populations show a higher risk for developing this condition than other ethnic groups. This is a rare condition.Secondary glaucoma occurs because of other eye conditions, such as uveitis (inflammation of the uvea: the middle layer of the eye), or eye injuries.Developmental (congenital) glaucoma is a serious abnormality of the eye. Usually, it develops at, or shortly after, birth. This is also a rare condition. Causes Most cases of glaucoma are caused by the increase in intraocular pressure resulting from the improper drainage of fluid within the eye, damaging the optic nerve. Although an exact cause has not yet been identified, certain factors have been reported to increase the risk for developing glaucoma:Age (glaucoma is more common with older age).Ethnicity (Caribbean, African, or Asian populations are at a higher risk).Family history.Other medical conditions, such as diabetes, hypertension, short-sightedness, and long-sightedness, may increase the risk for developing glaucoma. Symptoms Glaucoma rarely causes any symptoms. It develops slowly over several years, initially affecting the peripheral vision. Therefore, most people do not realise that they have glaucoma. This condition is often diagnosed only during a routine ophthalmic examination.The presence of the following symptoms may be observed:Blurry vision.Appearance of rainbow-coloured circles around bright objects/lights.Although both eyes are usually affected, glaucoma may be more severe in one eye. Occasionally, the sudden development of glaucoma has been noted along with the following symptoms:Redness.Blurred vision.Intense eye pain.Tenderness around the eyes.Appearance of rings around lights or bright objects.Headache, nausea, and vomiting. Diagnosis Glaucoma is diagnosed by two main tests:Optical coherence tomography (OCT) of the optic nerve head to rule out structural changes and thinning or loss of the retinal nerve fibre.Perimetry or Humphrey Field Analyser (HFA) to assess the peripheral visual field. Treatment Any loss of vision that has occurred before glaucoma is diagnosed cannot be reversed. However, specific glaucoma treatment methods can help stop the worsening of vision.The recommended treatment depends on the type of glaucoma and includes:Anti-glaucoma eyedrops to reduce the intraocular pressure.Laser treatments to reverse the blockage of drainage tubes or reduce fluid production within the eye.Trabeculectomy: A type of surgery to enhance the drainage of fluid out of the eye and reduce the intraocular pressure.Microinvasive glaucoma surgery (MIGS): A type of minimally invasive eye surgery in which the intraocular pressure is lowered via the creation of small incisions. This procedure improves the natural drainage, unlike the case for traditional glaucoma surgeries, in which the drainage system is bypassed. Read more about Glaucoma Filter Alphabet G
Dry Eye Syndrome Dry Eye Syndrome Home Overview Dry eye syndrome refers to a condition resulting from the eyes being unable to produce enough tears or the tears evaporating too quickly. This causes the eyes to dry out and eventually become inflamed. The incidence of dry eye syndrome increases with ageing, especially in women. Around 33% of people aged > 65 years may have this condition. Dry eye syndrome is common in patients with blepharitis and/or connective tissue disorders and among contact lens users.Tears are important as the tear film (the layer formed by tears at the front of the eye) not only lubricates the eyes, keeping them moist, but also plays a role in focusing the light into the eye.The tear film comprises three layers, each with different functions:The mucin layer (closest to the eye): It coats the cornea (the dome-shaped clear front layer of the eye), forming a foundation for the other layers.The aqueous layer (middle layer): It is mainly made of water and is the layer that is most associated with ‘tears.’ It is produced by the lacrimal (tear) gland and nourishes the cornea, providing it with oxygen, moisture, and other important nutrients.The lipid layer (outer layer): This is an oily film that seals the tear film, preventing the evaporation of the aqueous layer.The mucin and lipid layers are produced by small glands around the eye. When we blink, the tears are evenly spread over the front of the eye. The puncta (tiny drainage holes on the inside of the eyelids) drain away the excess tears, channelling them into the nose. This phenomenon explains why people often experiencing a runny nose while crying. Causes Several causes of dry eye syndrome have been identified:Occurs mostly as a consequence of the natural ageing process.Blinking problems.Problems with tear gland function, such as meibomian gland dysfunction.Some drugs, such as antihistamines and oral contraceptives, can cause dry eye.Using contact lenses may exacerbate (worsen) dry eye.Sometimes, dry eye represents a symptom of conditions affecting other body parts (particularly, Sjogren's syndrome or arthritis). Sjogren's syndrome is a chronic autoimmune condition marked by a dry mouth and dry vagina (apart from dry eyes). This condition may also be associated with certain types of arthritis. Symptoms Eye irritation, including itchiness, dryness, and discomfort in the eyes.Redness and a burning, stinging, or gritty sensation in the eyes.Temporary episodes of blurry vision, which normally go away with blinking or after a short time period.Sometimes, excessive watering from the eyes.Often, the eyes do not feel dry, but there are no tears during crying or when peeling onions. Diagnosis No single test that can diagnose dry eye has been established. However, ophthalmologists may perform certain procedures to diagnose this condition:Comprehensive eye examinations: Eye examinations that include a comprehensive assessment of the overall ocular and general health are performed.Schirmer tear test to measure the tear volume: Blotting paper strips are placed under the lower eyelids for five minutes to measure the extent to which the strips are soaked by the tears. The tear volume may also be measured via the phenol red thread test. In this test, a thread filled with phenol red (a pH-sensitive dye that changes colour upon contact with tears) is placed over the lower eyelid. After the thread is wetted by tears for about 15 seconds, the tear volume is measured.Staining tests to determine the tear quality: Eye drops containing special dyes are administered to determine the surface condition of your eyes. Corneal staining patterns are then examined, and the time required for the tears to evaporate is measured.Tear osmolarity test: The tear composition (levels of water and particles in tears) is measured. Reduced levels of water in the eyes are indicative of dry eye disease.Assessment of markers: The levels of dry eye disease-specific markers (such as decreased lactoferrin levels or elevated matrix metalloproteinase-9 levels) are measured. Treatment Artificial tears/tear substitutes: Over-the-counter artificial tears are often helpful in treating mild or moderate-stage dry eye syndrome. However, for patients with severe dry eye disease who need to use eye drops frequently (more than 6 times a day) or for patients who are contact lens users, preservative-free eye drops are recommended.Eye ointments can help lubricate the eyes. However, these are best used at night as they often cause blurred vision.Using the LipiFlow device (an FDA-approved procedure for Meibomian gland dysfunction).Lacrimal punctal plugs may be required to treat severe cases of dry eye syndrome. Read more about Dry Eye Syndrome Filter Alphabet D