Periventricular leukomalacia (PVL) is a kind of brain injury that mostly affects very premature babies. The injury happens in the white matter near the brain’s fluid-filled spaces called ventricles. “Peri-ventricular” means “around the ventricles,” and “leuko-malacia” means “softening of white matter.” In PVL, some white-matter cells die or are damaged. This can leave tiny soft areas or small cysts (little holes) in the white matter. Over time, this loss of white matter can lead to movement, learning, vision, or behavior problems as the child grows.
PVL usually happens because the white matter in very premature babies is fragile and still developing. Two main forces drive the injury:
Low blood flow or low oxygen to the periventricular area (ischemia/hypoxia), and
Inflammation that damages immature support cells called pre-oligodendrocytes (these cells would normally make myelin, the coating that helps brain signals travel fast). These vulnerable cells are easily hurt by poor blood flow, low oxygen, and inflammatory chemicals, so the white matter around the ventricles is the first to suffer. PMCPubMedNature
In the modern neonatal era, large cystic injuries (cystic PVL) are less common than before, but small, diffuse white-matter injuries are still frequent in very preterm infants. MRI can show these subtle injuries even when ultrasound looks normal.
Types of PVL
Cystic PVL (cPVL)
This type shows small cysts (fluid-filled spaces) in the white matter near the ventricles. Cysts appear after tissue death and can be seen on ultrasound or MRI. Babies with many or large cysts often have higher risk of movement problems later.Non-cystic / Diffuse PVL (diffuse white-matter injury)
This type does not make big cysts. Instead, the white matter looks abnormally bright or altered on MRI and may be thinner over time. It can be missed on early ultrasound but shows well on MRI, especially with diffusion or advanced techniques.“End-stage” or chronic PVL appearance
Months later, scans can show enlarged ventricles with wavy, irregular edges, loss of periventricular white matter, and thinning of the corpus callosum (the bridge between the two brain halves). These are signs that earlier white-matter injury healed with tissue loss.
Causes
PVL does not have one single cause. It usually comes from several stressors that reduce blood flow or oxygen to the fragile preterm white matter, or that trigger inflammation. Here are 20 well-supported causes or contributors:
Extreme prematurity (<32 weeks) – the white matter is very immature and easy to injure.
Very low birth weight (<1500 g) – goes along with prematurity and higher brain-injury risk.
Low brain blood flow or low oxygen (ischemia/hypoxia) – the main pathway to injury.
Infection and inflammation inside the womb (chorioamnionitis) – inflammatory chemicals can hurt white matter. PubMed
Inflammation of the umbilical cord (funisitis / fetal inflammatory response) – shows a strong fetal inflammatory state tied to brain injury. SSRN
Prolonged rupture of membranes (PROM/PPROM) – raises infection and inflammation risk. PubMed
Neonatal sepsis (blood infection after birth) – systemic inflammation can damage white matter.
Necrotizing enterocolitis (NEC) – severe gut inflammation spills over and is linked to white-matter injury and worse outcomes.
Mechanical ventilation with low carbon dioxide (hypocarbia) – over-ventilation can cause brain vessel narrowing and white-matter injury.
Large swings in oxygen levels (hyperoxia/hypoxia) – early oxygen extremes stress fragile white matter.
Low blood pressure or unstable circulation – reduces steady brain perfusion in preterm infants.
Cerebral blood-flow regulation that is not yet mature – preterm brains cannot auto-regulate well, so pressure or gas changes hit harder.
Repeated apnea and bradycardia episodes – repeated short drops in oxygen and blood flow add up. (Risk factor reviews of preterm white-matter injury include these events.)
Periventricular hemorrhagic infarction or severe IVH nearby – venous congestion and tissue infarction can extend into periventricular white matter.
Patent ductus arteriosus with hemodynamic effects – can disturb systemic and cerebral blood flow in very preterm infants. (Reviewed among risk factors for preterm white-matter injury.)
Anemia and low oxygen-carrying capacity – less oxygen delivery may worsen ischemic vulnerability in very preterm infants. (Discussed within broader preterm WMI mechanisms.)
Oxidative stress – immature white-matter cells are sensitive to free radicals during illness, resuscitation, or oxygen swings. PMC
Cytokine-driven microglial activation – inflammation activates brain immune cells that damage pre-oligodendrocytes.
Early postnatal cerebral oxygenation instability – abnormal variability by near-infrared spectroscopy (NIRS) relates to later brain injury.
Overall “multiple hits” in the NICU – studies show that repeated inflammatory episodes (sepsis/NEC) raise the risk of poor neurodevelopment far more than a single episode.
Common symptoms and signs
PVL may not show clear signs right away. Some signs appear in the NICU; others appear as the child grows. Here are 15 plain-English symptoms and signs doctors and parents watch for:
Low or high muscle tone in early months – babies can be floppy at first or later become stiff. Medscape
Spasticity (especially in the legs) – tight, scissoring legs or stiff movements, often called spastic diplegia.
Delayed motor milestones – late head control, rolling, sitting, or walking.
Abnormal reflexes – persistent primitive reflexes or very brisk stretch reflexes. Toronto Centre for Neonatal Health
Poor head control – head may lag when pulled to sit. Toronto Centre for Neonatal Health
Feeding difficulties – weak suck, poor coordination, or choking episodes. Medscape
Apnea and bradycardia in the NICU – pauses in breathing and slow heart rate can be part of the picture in very preterm babies with brain vulnerability.
Seizures – some infants with PVL have seizures in the neonatal period or later.
Vision problems – poor visual tracking, strabismus, or difficulty keeping steady gaze; white-matter injury is linked with impaired gaze. VIVO
Hearing concerns – high-risk preterm infants often need hearing checks because white-matter injury can coexist with auditory pathway issues.
Coordination and balance issues – clumsy movements or trouble with fine motor skills later in childhood.
Learning and cognitive delays – difficulties with attention, processing, or school learning can appear years later.
Behavior or sensory challenges – some children show sensory-processing or behavior differences as they grow.
Small head growth over time – some children show slower head-circumference growth linked to underlying brain growth issues.
Speech and language delay – challenges with early communication skills may appear in toddlers.
Diagnostic tests
A) Physical exam tests
Comprehensive newborn neurological exam
The clinician checks posture, tone, movements, and basic reflexes. This exam helps spot early concerns and guides which babies need closer follow-up and imaging. Toronto Centre for Neonatal HealthPrimitive reflex check (Moro, grasp, rooting)
Doctors look for reflexes that should fade with age. Reflexes that are still strong or very brisk later on can signal white-matter injury. Toronto Centre for Neonatal HealthVisual tracking and gaze assessment
Watching how the baby fixes and follows a face or object can reveal early visual pathway problems seen with white-matter injury. VIVOHead-circumference measurement over time
Regular head growth checks are quick and helpful to track brain growth. Slower-than-expected growth can prompt further evaluation.
B) Manual developmental tests
General Movements Assessment (GMA)
A trained observer reviews a brief video of the baby’s spontaneous fidgety movements. Absent or abnormal fidgety movements strongly predict a later motor disorder such as cerebral palsy, especially in preterm babies.Hammersmith Neonatal Neurological Examination (HNNE)
A standardized bedside exam used near term-equivalent age. It has moderate accuracy to flag infants who may develop motor problems and who need MRI and close follow-up.Hammersmith Infant Neurological Examination (HINE)
A simple, scorable exam from 2 to 24 months. Low scores at 3–12 months are strongly linked with cerebral palsy risk and cognitive delay; it is widely used to track high-risk infants after PVL.Test of Infant Motor Performance (TIMP)
A structured motor test used in the first months of life. It complements HNNE/HINE to describe early motor control and to identify babies who need therapy and imaging.
C) Laboratory & pathological tests
Placental pathology (looking for chorioamnionitis or funisitis)
Examining the placenta and umbilical cord after birth can prove an inflammatory cause that is linked to white-matter injury risk in the baby. PubMedInflammatory markers (e.g., IL-6 in cord blood, CRP)
High fetal or neonatal inflammatory markers support the idea of a fetal inflammatory response that can damage white matter. SSRNNeonatal sepsis work-up (blood cultures ± procalcitonin/CRP)
Since sepsis can trigger brain injury through inflammation, proving or excluding infection helps with PVL risk assessment and care. NatureBlood gas analysis (PaCO₂ and oxygen levels)
Very low CO₂ (hypocarbia) and oxygen extremes are linked to white-matter injury. Blood gases guide safe ventilation to protect the brain.
D) Electrodiagnostic tests
Standard EEG (electroencephalogram)
Records brain waves to detect seizures and to assess background brain function in high-risk newborns.Amplitude-integrated EEG (aEEG)
A simplified bedside EEG that tracks brain background activity, sleep-wake cycling, and seizures over hours to days; helpful for risk and prognosis when combined with imaging.Visual Evoked Potentials (VEP)
Measures the brain’s response to a light flash. It helps assess the visual pathways, which can be affected with white-matter injury. ScienceDirectAuditory Brainstem Response (ABR/BAER)
Measures the hearing nerve and brainstem response to sound; useful because hearing pathways can also be vulnerable in very preterm infants. IOVS
E) Imaging tests
Screening cranial ultrasound (cUS)
Bedside ultrasound is safe, repeatable, and the first-line test in very preterm infants. It detects IVH and many cystic white-matter injuries; it is part of routine screening protocols in the NICU. NCBISerial ultrasound at key time points
Because injuries can evolve, guidelines advise scanning early (first 7–10 days) and again closer to term-equivalent age to catch later-appearing white-matter abnormalities. NCBIConventional brain MRI at term-equivalent age (TEA)
MRI is more sensitive than ultrasound for subtle white-matter injury and gives a better map of injury burden and prognosis.Diffusion-based MRI (DWI/DTI)
DWI can show early PVL changes in the first weeks, even before cysts appear. DTI measures microstructure (like fractional anisotropy) to reveal white-matter abnormalities and track development. ScienceDirectPubMedNature
Non-pharmacological treatments
(For each: what it is, why, and how it helps.)
Early intervention therapy (start in infancy): a home-and-clinic program blending PT/OT/speech. Purpose: build skills during the brain’s most “plastic” years. Mechanism: repetitive, play-based practice strengthens surviving circuits and helps new ones form.
Physical therapy (PT): stretches, strength, posture, mobility training. Purpose: reduce stiffness, improve balance and walking. Mechanism: task-specific practice remodels motor pathways.
Occupational therapy (OT): hand use, dressing/feeding skills, sensory strategies. Purpose: independence in daily activities. Mechanism: graded tasks shape fine-motor networks.
Speech-language therapy: feeding/safe swallow, communication (including AAC devices). Purpose: safer eating and clearer communication. Mechanism: targeted oromotor training and language mapping.
Constraint-induced movement therapy (CIMT) in toddlers: briefly “constrains” the stronger limb to train the weaker one with fun tasks. Purpose: improve hand use on the affected side. Mechanism: intensive, goal-directed repetition.
Vision rehabilitation: contrast toys, lighting, and orientation training for cortical visual impairment. Purpose: better functional seeing and navigation. Mechanism: repeated, structured visual tasks strengthen processing.
Hearing support: timely diagnostic ABR and, if needed, hearing aids/therapy. Purpose: clear access to sound for speech development. Mechanism: amplifies input during key language windows.
Developmental “cue-based” feeding programs: pacing, positioning, thickened textures when indicated. Purpose: safer, less tiring feeds and better growth. Mechanism: matches infant cues, reduces aspiration.
Positioning and 24-hour posture care: adaptive seating, sleep positioning, standing frames. Purpose: comfort, prevent contractures and hip problems. Mechanism: maintains muscle length and joint alignment; supports bone health.
Orthotics (AFOs, SMOs): braces to guide foot/ankle alignment. Purpose: improve standing/walking efficiency. Mechanism: external support reduces spastic pull.
Serial casting: short-term casts to gently lengthen tight muscles (e.g., calf). Purpose: improve range and gait. Mechanism: low-load, long-duration stretch.
Spasticity management without meds: heat, stretching programs, vibration platforms (where available). Purpose: comfort and motion. Mechanism: sensory input modulates spinal reflexes.
Hydrotherapy/therapy in warm water: buoyancy and warmth help movement. Purpose: easier practice with less pain/tone. Mechanism: reduces gravitational load, may reduce spasticity temporarily.
Parent coaching & mental-health support: training plus counseling. Purpose: confident caregiving, less stress. Mechanism: skills + support improve follow-through and child outcomes.
Assistive technology (AT): seating systems, walkers, communication devices. Purpose: participation at home/school. Mechanism: bypasses physical bottlenecks to learning.
Early education and inclusive preschool: Individualized Education Plans. Purpose: build cognitive, language, social skills. Mechanism: enriched, repetitive, peer-supported learning.
Bone health program: weight-bearing (standing frames), vitamin D and calcium as advised. Purpose: stronger bones; fewer fractures. Mechanism: mechanotransduction during growth.
Hip surveillance program: regular hip checks and X-rays in children with CP (especially non-walkers). Purpose: catch hip migration early and treat before painful dislocation. Mechanism: standardized schedule triggers timely ortho referral.
Nutrition optimization with human milk and appropriate fortification in the NICU: Purpose: better overall outcomes, possibly less white-matter injury risk; supports immunity and growth. Mechanism: bioactive factors, optimal fats (including DHA/ARA), and tailored calories.
Routine vision/hearing surveillance through infancy: early detection → early action. Mechanism: serial ABR/VEP and behavioral testing guide timely supports.
Drug treatments
Important safety note: doses for infants and children must be individualized by specialists. The ranges below are for general context only—your care team will decide what fits your child.
Phenobarbital (antiseizure; first-line in neonates)
Class: barbiturate ASM. Typical NICU loading: ~20 mg/kg IV (may repeat once); maintenance is individualized. Purpose: stop neonatal seizures linked to brain injury. How it works: enhances GABA signaling to quiet overactive neurons. Side effects: sedation, breathing depression, hypotension; long-term use monitored.Levetiracetam (antiseizure; often second-line)
Class: ASM. Typical NICU load: ~40–60 mg/kg IV; maintenance individualized. Purpose: backup if seizures persist. How it works: binds SV2A to stabilize neurotransmitter release. Side effects: sleepiness, irritability; overall favorable profile. (Phenobarbital remains first-line in most guidelines.)Fosphenytoin/Phenytoin (second-line ASM)
Class: sodium-channel ASM. Typical load: ~20 mg/kg IV equivalent; maintenance individualized. Purpose: control persistent seizures. Side effects: arrhythmias/hypotension (monitor), rash; levels monitored.Intrathecal Baclofen (ITB) via pump (for severe spasticity in older children)
Class: GABA-B agonist muscle relaxant delivered into spinal fluid. Dosing: test dose via lumbar puncture; then implanted pump with programmable continuous infusion. Purpose: reduce severe generalized spasticity when oral meds fail. Side effects: overdose/withdrawal risks if pump issues; requires specialist center.Oral Baclofen (spasticity)
Class: GABA-B agonist. Typical pediatric start: low dose divided TID and titrated slowly per weight/response (specialist dosing). Purpose: reduce tone/spasms. Side effects: sleepiness, weakness; taper if stopping.Diazepam (spasticity, short-term or night-time spasms)
Class: benzodiazepine. Use: short courses for procedures/night spasms; pediatric dosing individualized. Side effects: sedation, dependence with prolonged use; caution.Botulinum toxin type A (focal spasticity)
Class: neuromuscular blocker injected into tight muscles. Dosing: unit/kg limits by product and total body weight; spaced every ~3 months as needed. Purpose: relax over-active muscles to improve range and function. Side effects: local weakness, rare systemic effects; best in expert hands with therapy program. aacpdm.orgAnalgesics/antispasmodic adjuncts (e.g., acetaminophen; careful use of others)
Purpose: comfort to enable therapy and sleep. Note: avoid routine NSAIDs in fragile infants unless directed.Anti-reflux meds when feeding issues cause pain/aspiration risk
Class: acid suppression/other agents as indicated. Purpose: protect airway and growth; chosen after feeding evaluation.Vitamin D and iron supplements (as prescribed)
Purpose: bone health and anemia prevention in children with CP/feeding limitation. Mechanism: supports growth and participation in therapy. (Given per pediatric guidelines.)
Why these are “supportive”: medications treat complications (spasticity, seizures, discomfort), not the underlying white-matter injury. Guidelines continue to evolve on when to start, stop, and combine these therapies—your pediatric neurology/rehab team will guide timing. PMC
Dietary “molecular” supplements
(Always use only what your pediatrician/dietitian advises for your child.)
Human milk (mother’s own or donor; with fortifier for preterm infants): supports immunity, gut health, and neurodevelopment; may protect the vulnerable white matter. Mechanism: bioactive proteins, HMOs, DHA/ARA, antioxidants.
DHA/ARA as part of medically guided fortification: long-chain omega-3/6 fats important for myelin and vision. Evidence for extra-high dosing is mixed; follow NICU protocol.
Choline (within prescribed feeds): building block for cell membranes/myelin and neurotransmitter (acetylcholine). Mechanism: supports membrane/myelin synthesis.
Vitamin D: bone health; may support muscle function.
Iron (if needed): prevents anemia that can sap energy and attention.
Zinc: supports immune function and growth when deficient.
Iodine (adequate intake): needed for thyroid hormones that drive brain development.
Lutein/zeaxanthin (in some preterm formulas/fortifiers): retinal and possibly neural antioxidant support.
Protein-energy fortification (preterm-specific): to meet higher growth needs, protecting brain and body.
Fiber and fluids (as age-appropriate): prevent constipation that worsens discomfort and spasticity.
(Key point: human milk with appropriate fortification is the strongest nutrition foundation for preterm infants; individual “add-on” supplements should be clinically indicated rather than routine.)
Regenerative / stem-cell–type
There is no approved “immunity booster” to treat PVL. Two preventive antibody options protect fragile infants from a serious lung virus (RSV), which indirectly helps keep babies healthier while developing.
Nirsevimab (RSV preventive antibody)
Dose: single shot—50 mg if <5 kg, 100 mg if ≥5 kg (first RSV season); higher dose for certain high-risk kids in second season. Function: passive immunity to RSV to prevent hospitalization. Status: recommended by CDC/ACIP and AAP.Palivizumab (RSV preventive antibody for select high-risk infants when nirsevimab not available/eligible)
Dose: 15 mg/kg monthly during RSV season. Function: reduces severe RSV in specific high-risk groups. Status: older standard; now mainly for defined indications.Umbilical cord blood / mesenchymal stem cells (MSCs) – experimental
Function: aim to reduce inflammation and promote repair. Mechanism: trophic factors/exosomes; possible support for oligodendrocyte maturation. Status: early trials and meta-analyses suggest small improvements in motor scores in children with CP; not standard care; dosing varies by trial; only within regulated clinical trials.MSC-derived exosomes – experimental
Function/mechanism: cell-free vesicles carrying growth and anti-inflammatory signals; promising in animal models of preterm white-matter injury. Status: preclinical/early research.Erythropoietin (EPO) – investigational neuroprotection
Function: anti-inflammatory and pro-maturation signals in brain; mixed clinical results; not standard for PVL prevention/treatment. Status: research use only under protocols.Melatonin or other anti-inflammatory neuroprotectants – investigational
Function: antioxidant/anti-inflammatory effects; Status: small studies only; not standard.
Surgeries
Not every child will need surgery. These options are for specific complications:
Selective Dorsal Rhizotomy (SDR): neurosurgeon cuts a small portion of sensory nerve rootlets in the lower spine. Why: reduce severe leg spasticity in carefully selected children to improve comfort and mobility, alongside intensive rehab. aacpdm.org
Intrathecal Baclofen Pump (implant): device that delivers baclofen into spinal fluid. Why: treat generalized severe spasticity when oral meds are ineffective or not tolerated.
Orthopedic soft-tissue procedures (e.g., tendon lengthening) and bony surgery (e.g., hip reconstruction): Why: correct contractures, improve hip alignment, reduce pain, and ease care in children with CP from PVL. Timing is guided by hip surveillance findings.
Gastrostomy tube (G-tube): surgically placed feeding tube. Why: when oral intake is unsafe or insufficient, a G-tube secures nutrition and reduces aspiration risk.
Ventriculoperitoneal (VP) shunt for post-hemorrhagic hydrocephalus (if present): Why: drain extra brain fluid that can build up after severe IVH; many infants with persistent hydrocephalus require permanent shunting.
Prevention strategies
(Many are obstetric/NICU actions—parents can ask their team about these.)
Prevent prematurity when possible via good prenatal care.
Antenatal corticosteroids for mothers at risk of preterm delivery—reduce serious newborn complications.
Antenatal magnesium sulfate for fetal neuroprotection when very preterm birth is expected—reduces the risk of cerebral palsy in survivors.
Prevent/treat maternal infections (e.g., chorioamnionitis) promptly.
Gentle ventilation and stable CO₂ levels in the NICU—avoid hypocapnia, which is linked to PVL and CP.
Targeted oxygen levels—avoid both low oxygen and hyperoxia, which can injure the brain and eyes.
Hemodynamic stability: careful fluid/blood pressure management to keep brain blood flow steady.
Human milk feeding with fortification to support brain, gut, and immunity.
Prevent sepsis (strict hand hygiene, central-line bundles, breast milk).
Standard hearing/vision surveillance—early detection allows early intervention.
When to see the doctor urgently
Any seizures (staring spells, rhythmic jerks, unusual stiffening).
Feeding trouble with coughing/choking, poor weight gain, or dehydration.
Sudden change in muscle tone, unusual sleepiness, vomiting with bulging soft spot (could be hydrocephalus).
New vision/hearing concerns or loss of skills already learned.
Your pediatrician, neurologist, physiatrist, therapists, and dietitian are your first stop; they will coordinate referrals.
What to eat and what to avoid
(For infants, follow your pediatrician/NICU dietitian; for older kids with CP, texture and safety matter.)
Do choose human milk or preterm-appropriate formula with fortifiers as prescribed.
Do use texture-modified foods (purees/soft solids) if chewing is hard; protect airway.
Do offer small, frequent feeds if fatigue limits intake.
Do keep vitamin D, calcium, iron on plan per clinician advice.
Do encourage fiber and fluids (age-appropriate) to prevent constipation.
Avoid choking hazards (nuts, hard raw veggies) until safe.
Avoid excess added sugar/salt—empty calories displace needed nutrition.
Avoid honey under 1 year (botulism risk).
Avoid large, tiring meals—use pacing and breaks.
Avoid unproven supplements marketed as “brain boosters”; discuss everything with your clinician first.
Frequently asked questions
1) Can PVL be cured?
Not with a medicine or operation. But function can improve a lot with early, consistent therapy, good nutrition, and smart spasticity/seizure management.
2) Will my child walk or talk?
Many children with PVL do walk and talk, especially with early therapy. Abilities vary by how much white matter was injured and where.
3) Is PVL the same as cerebral palsy (CP)?
No. PVL is a type of brain injury; CP is the movement disorder that can result. Many but not all children with PVL develop CP.
4) How is PVL found?
With cranial ultrasound in the NICU and often an MRI at term-equivalent age, plus early movement exams (GMA/HINE).
5) Why did PVL happen to my baby?
Usually a mix of prematurity, blood-flow/oxygen fluctuations, and inflammation around birth—risk factors that doctors work hard to reduce.
6) What therapies matter most right now?
Early intervention—PT/OT/speech, feeding support, and vision/hearing services—started as soon as possible.
7) Are there medicines that repair the brain?
Not yet. Medicines treat symptoms (seizures, spasticity, reflux, sleep). Research into regenerative approaches is ongoing but not standard care.
8) Should we try stem cells?
Only within regulated clinical trials. Current studies show small improvements and short-term safety, but more high-quality trials are needed before routine use.
9) Is human milk really that important?
Yes—human milk is linked with better overall outcomes in preterm infants and may help protect the vulnerable white matter; fortification is often needed for growth.
10) Could seizures appear later?
Yes; seizures can occur at any point. Report any concerning events; phenobarbital is usually the first-line neonatal choice, with other options later if needed.
11) How do we prevent hip problems?
Enroll in a hip surveillance program if your child has CP—regular checks and X-rays catch hip migration early so it can be treated.
12) What about RSV season?
Ask about nirsevimab (or palivizumab if indicated) to reduce RSV hospitalization risk—important for fragile infants.
13) Will my child need a feeding tube?
Some children benefit from a G-tube when oral intake is unsafe or inadequate; it can improve growth and reduce stress around meals.
14) Why are CO₂ and oxygen targets a big deal in the NICU?
Too-low CO₂ (hypocapnia) and too-high oxygen (hyperoxia) can harm the preterm brain; teams tightly regulate ventilator and oxygen settings.
15) What’s the long-term outlook?
Outcomes range widely. With early diagnosis and family-centered therapy, many children gain meaningful skills and quality of life. Celebrate progress—big and small.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: August 14, 2025.
