Dyke Davidoff Masson Syndrome

Overview

• Definition: Dyke-Davidoff-Masson Syndrome (DDMS), also known as cerebral hemiatrophy or cerebello-parenchymal hemiatrophy, is a rare neurological disorder characterized by unilateral cerebral hemiatrophy, often accompanied by contralateral hemiparesis or hemiplegia, seizures, intellectual disability, and facial asymmetry. The condition results from an insult to one cerebral hemisphere during early development, typically prenatal or perinatal, leading to a cascade of compensatory changes in the skull and brain.

• Epidemiology: DDMS is rare, with no precise incidence or prevalence rates firmly established. It affects males more frequently than females and typically manifests in childhood. Reports suggest that it can account for a significant proportion (e.g., 20-30%) of cases labelled as unexplained hemiplegia in children. It does not appear to have a specific geographical or ethnic predisposition.

• Classification:

  • Congenital DDMS: Occurs due to insults during the prenatal or perinatal period, often within the first 3 years of life. This is the more common form, characterized by evidence of widespread cerebral injury and secondary bony changes in the skull.
  • Acquired DDMS: Results from a unilateral cerebral injury later in childhood or adulthood, usually from trauma, infection (e.g., encephalitis, meningitis), vascular events (e.g., arterial infarction, venous thrombosis), or prolonged status epilepticus. The bony changes are often less pronounced or absent compared to the congenital form, depending on the age of onset of the insult.

Pathophysiology

• Mechanism: The fundamental mechanism involves a significant unilateral brain injury, typically ischemic, hypoxic, or traumatic, occurring during a critical period of brain development (prenatal or early postnatal). This injury leads to:

  1. Unilateral Cerebral Atrophy: Loss of brain parenchyma on one side, affecting cortical gray matter, subcortical white matter, and often the ipsilateral cerebellar hemisphere (crossed cerebellar diaschisis).
  2. Compensatory Skull Changes: The ipsilateral cerebral atrophy reduces the overall volume of the affected hemisphere. To fill this void and equalize intracranial pressure, compensatory changes occur over time:
     • Ipsilateral Ventriculomegaly: Dilation of the lateral ventricle on the affected side.
     • Thickening of the Ipsilateral Calvarium: The skull bone over the atrophic hemisphere thickens.
     • Elevation of the Ipsilateral Petrous Ridge: The petrous part of the temporal bone may be elevated.
     • Expansion of the Ipsilateral Air Sinuses: Hypertrophy of the frontal sinus, ethmoid sinus, and sphenoid sinus on the affected side.
     • Deviation of the Falx Cerebri and Tentorium: Shift towards the atrophic side.
  3. Contralateral Neurological Deficits: The atrophied brain hemisphere results in damage to descending motor pathways, leading to contralateral motor deficits (hemiparesis or hemiplegia).
  4. Epileptogenesis: The injured brain tissue can become epileptogenic, leading to chronic seizures.
  5. Cognitive Impairment: Varying degrees of intellectual disability can occur due to the extent and location of brain damage.

• Risk Factors:

  • Congenital/Perinatal:
    • Intrauterine infections (e.g., TORCH infections)
    • Perinatal asphyxia or hypoxic-ischemic encephalopathy
    • Intrauterine stroke or arterial/venous infarction
    • Trauma during birth
    • Genetic predisposition (rare, but some syndromes like Sturge-Weber can mimic aspects)
  • Acquired:
    • Head trauma (especially severe unilateral injury)
    • Central nervous system infections (e.g., viral encephalitis, bacterial meningitis leading to vasculitis)
    • Vascular events (e.g., large vessel infarction, venous sinus thrombosis, hemorrhage)
    • Prolonged status epilepticus in childhood (e.g., Rasmussen encephalitis as a precursor)

• Protective Factors: There are no known protective factors once the initial insult has occurred. Early recognition and aggressive management of the underlying cause (e.g., prompt treatment of infections, prevention of perinatal asphyxia) may mitigate the severity of brain damage, but cannot prevent the syndrome if significant injury has already occurred.

Clinical Presentation

Signs and Symptoms

• Cardinal Features:

  • Contralateral Hemiparesis/Hemiplegia: Weakness or paralysis on the side of the body opposite to the cerebral atrophy. This is often present from infancy or early childhood.
  • Seizures: Common, often refractory to antiepileptic drugs. Can be focal, secondarily generalized, or infantile spasms.
  • Intellectual Disability: Ranges from mild to severe, correlated with the extent of brain damage.
  • Facial Asymmetry: Hypoplasia of the facial muscles on the ipsilateral side of the body (contralateral to the brain atrophy), or ipsilateral facial atrophy due to disuse or trophic changes.

• Early Signs (Infancy/Early Childhood):

  • Delayed developmental milestones (motor, cognitive, speech).
  • Infantile spasms or other types of seizures.
  • Asymmetrical motor activity (e.g., preferential use of one hand, asymmetry in crawling or walking).
  • Head tilt or deviation.
  • Subtle facial asymmetry.

• Advanced Signs (Later Childhood/Adulthood):

  • Established contralateral hemiparesis with spasticity, contractures, and gait abnormalities.
  • Refractory epilepsy, potentially leading to secondary injuries.
  • Well-defined intellectual disability and learning difficulties.
  • Pronounced facial asymmetry.
  • Speech and language disorders (dysarthria, aphasia, depending on the affected hemisphere).
  • Behavioral problems, mood disorders.
  • Headache (less common, but can occur).

• Atypical Presentations:

  • Bilateral involvement (rare, typically asynchronous or severe global insult).
  • Minimal or no intellectual disability (in cases with highly localized damage or adequate compensatory mechanisms).
  • Seizure-free patients (uncommon, but possible).

Physical Examination

• Inspection:

  • Facial Asymmetry: Atrophy of facial muscles (sometimes hypertrophy of contralateral muscles due to increased use).
  • Body Asymmetry: Smaller limbs and muscles on the contralateral hemiparetic side; often with contractures.
  • Head Size/Shape: Mild microcephaly, especially over the atrophic hemisphere, or subtle skull flattening.
  • Gait: Hemiparetic gait, circumduction of the affected leg.
  • Eye/Speech: Strabismus, nystagmus (less common), dysarthria.

• Palpation:

  • Palpable skull thickening on the side of hemiatrophy (ipsilateral to the brain atrophy).
  • Muscle tone: Spasticity, especially in the contralateral limbs.

• Special Tests:

  • Neurological Examination:
    • Detailed assessment of motor power, tone, reflexes (hyperreflexia, clonus on contralateral side, extensor plantar response).
    • Sensory examination (may be impaired).
    • Cranial nerve examination (facial asymmetry, tongue deviation, visual field deficits).
    • Coordination and balance.
  • Neuropsychological Assessment: To quantify cognitive deficits and intellectual disability.

Diagnostic Approach

History Taking

• Key Questions:

  • Perinatal History: Any complications during pregnancy, birth (e.g., prematurity, asphyxia, infections, trauma)?
  • Developmental Milestones: Age of onset of motor, language, and cognitive delays.
  • Seizure History: Age of onset, seizure type, frequency, duration, response to medication.
  • Progressive Weakness/Symptoms: Is the condition stable or worsening? (Important for differentiating acquired progressive conditions like Rasmussen's)
  • Associated Symptoms: Feeding difficulties, behavioral changes, visual problems.
  • Family History: Any similar conditions or neurological disorders.
  • Previous Investigations: Any prior imaging, EEG, or genetic tests.

• Red Flags:

  • Acute onset of hemiparesis or seizures in a previously healthy child (suggests acquired cause, e.g., stroke, infection).
  • Progressive neurological deterioration (e.g., Rasmussen encephalitis, primary mitochondrial disorders).
  • New focal neurological deficits or worsening seizure control.

Laboratory Tests

• First-Line: No specific laboratory tests diagnose DDMS itself, but they help rule out underlying treatable causes, especially in acquired cases.

  • Complete Blood Count (CBC) with differential: To exclude infection or inflammatory processes.
  • Electrolytes, Glucose, Renal/Liver Function Tests: Baseline assessment and seizure work-up.
  • CSF Analysis (if meningitis/encephalitis suspected): Cell count, protein, glucose, culture, PCR for viral pathogens.
  • Coagulation Profile, Thrombophilia Screen: If a vascular event is suspected (e.g., factor V Leiden, protein C/S deficiency, antiphospholipid antibodies).
  • Infectious Work-up (TORCH screen): In congenital cases where intrauterine infection is suspected.

• Confirmatory: No specific lab tests directly confirm DDMS; diagnosis is primarily radiological.

• Monitoring:

  • Antiepileptic Drug (AED) Levels: To optimize seizure control and monitor for toxicity.
  • Developmental Assessments: Regular follow-up to track cognitive and motor progress.

Imaging

• Recommended:

  • Cranial Computed Tomography (CT) Scan: Often the initial imaging modality due to availability and speed. Key findings:
    • Unilateral cerebral atrophy: Reduced brain volume on one side.
    • Ipsilateral ventriculomegaly: Dilation of the lateral ventricle on the affected side.
    • Compensatory skull changes:
      • Thickening of the ipsilateral calvarium.
      • Elevation of the ipsilateral petrous ridge.
      • Hypertrophy of ipsilateral paranasal sinuses (frontal, ethmoid, sphenoid) and mastoid air cells.
      • Deviation of the falx cerebri and tentorium towards the atrophic side.
    • May show evidence of old infarct or hemorrhage.
  • Magnetic Resonance Imaging (MRI) of the Brain: Provides superior soft tissue resolution and is the gold standard for defining the extent and nature of brain injury.
    • Confirms cerebral atrophy: Detailed visualization of cortical and subcortical volume loss.
    • Characterizes underlying lesions: Differentiates between old infarction, malformations, or gliosis.
    • Identifies T2/FLAIR hyperintensities: Indicative of gliosis or demyelination.
    • DWI/ADC sequences: Can assess for ongoing acute ischemic events.
    • MR Angiography/Venography (MRA/MRV): May be indicated to assess for vascular abnormalities (e.g., arterial occlusion, venous thrombosis) if the etiology is unclear.

• Advanced:

  • Functional MRI (fMRI): Can map critical functional areas (e.g., motor cortex, language areas) to aid in presurgical planning for epilepsy surgery.
  • Diffusion Tensor Imaging (DTI): To assess the integrity of white matter tracts and quantify connectivity issues.

• Electroencephalography (EEG): Essential for patients with seizures.

  • Findings: Slowing of background activity over the affected hemisphere, focal epileptiform discharges, or generalized discharges depending on seizure type. May show asymmetry in amplitude or frequency. Video-EEG monitoring can characterize seizure types and localize ictal onset zones.

Management

Acute Management

• Immediate (If acute onset or severe seizures):

  • Airway, Breathing, Circulation (ABC) assessment and support: As with any neurological emergency.
  • Management of Status Epilepticus:
    • First-line: Benzodiazepines (e.g., IV lorazepam 0.1 mg/kg; max 4 mg, repeated once if needed).
    • Second-line: Phenytoin (IV 20 mg/kg), fosphenytoin, levetiracetam (IV 20-50 mg/kg), valproic acid (IV 20-40 mg/kg).
    • Third-line: Continuous infusions (e.g., midazolam, propofol) in an ICU setting for refractory status epilepticus.

• Stabilization:

  • Address the underlying acute cause if identified (e.g., antibiotics for bacterial meningitis, antithrombotic therapy for acute stroke).
  • Control fever, manage electrolyte imbalances.
  • Pain management if applicable (e.g., post-traumatic).

• Emergency: Not typically a primary emergency syndrome itself unless presenting with acute complications like status epilepticus, acute stroke, or severe head trauma.

Chronic Management

• Pharmacological:

  • Antiepileptic Drugs (AEDs): The mainstay for seizure control. Choice depends on seizure type and patient profile. Often polytherapy is required due to refractory nature.
    • Commonly used (monotherapy or polytherapy): Levetiracetam, valproic acid, carbamazepine, oxcarbazepine, lamotrigine, topiramate, clobazam.
    • Dosing: Titrated based on clinical response and side effects. For example, Levetiracetam: initial 10-20 mg/kg/day in two divided doses, increasing weekly up to 60 mg/kg/day or higher.
  • Antispasticity Medications: For severe spasticity.
    • Oral baclofen (initial 5-10 mg BID/TID, slowly titrate to max 20 mg QID).
    • Tizanidine (initial 2 mg TID, usually 2-4 mg TID-QID, max 36 mg/day).
    • Botulinum toxin injections for focal spasticity and contracture management (e.g., into hamstring, gastrocsoleus muscles).

• Non-pharmacological:

  • Physical Therapy: Crucial for managing hemiparesis, spasticity, preventing contractures, improving gait, and maximizing functional independence. Starts early and continues lifelong.
  • Occupational Therapy: Focuses on activities of daily living (ADLs), fine motor skills, assistive technology, and adaptive strategies.
  • Speech and Language Therapy: For dysarthria, aphasia, or other communication difficulties.
  • Neuropsychological Rehabilitation: Cognitive training, behavioral management strategies, educational support.
  • Psychological and Social Support: For patients and families dealing with chronic illness, intellectual disability, and behavioral issues.
  • Special Education: Individualized Education Programs (IEPs) for children with intellectual disabilities.

Treatment Algorithms

• First-Line (Seizure Management):

  1. Initiate monotherapy with a broad-spectrum AED if seizure type is unknown or generalized (e.g., levetiracetam, valproic acid).
  2. If focal seizures, can use focal AEDs (e.g., carbamazepine, oxcarbazepine, lamotrigine).
  3. Titrate to effective dose or maximum tolerated dose.

• Second-Line (Seizure Management):

  1. If monotherapy fails, consider adding a second AED (polytherapy).
  2. Careful selection based on synergy and side effect profiles.

• Refractory Cases (Seizure Management):

  1. Strict criteria for refractory epilepsy: Failure of two appropriately chosen and dosed AEDs to control seizures.
  2. Epilepsy Surgery Evaluation:
     • Candidacy: Patients with persistent, debilitating seizures impacting quality of life, especially if imaging shows localized atrophy and EEG can localize a seizure focus to the affected hemisphere.
     • Procedures:
       • Hemispherectomy / Hemispherotomy: Functional disconnection of the affected hemisphere. This is often the most effective treatment for intractable seizures in DDMS when the affected hemisphere is largely non-functional. Prognosis for seizure freedom is high (e.g., 60-80%).
       • Corpus Callosotomy: Palliative procedure for generalized tonic-clonic or atonic seizures ("drop attacks"), reducing seizure spread but not achieving seizure freedom.
       • Vagus Nerve Stimulation (VNS): May be considered as an adjunctive therapy for intractable focal seizures not amenable to resective surgery.
  3. Ketogenic Diet: Can be considered, particularly in pediatric patients with refractory epilepsy not responding to AEDs or awaiting surgery.

Complications

• Common:

  • Refractory Epilepsy: Seizures that are difficult to control with medication, leading to impaired quality of life and potential for injury.
  • Neurodevelopmental Delays: Varies widely from mild learning difficulties to severe intellectual disability and global developmental delay.
  • Spasticity and Contractures: Leading to deformities, pain, and impaired mobility.
  • Behavioral and Psychiatric Issues: Attention-deficit/hyperactivity disorder (ADHD), aggression, anxiety, depression (especially in older children/adults).
  • Speech and Language Disorders.

• Serious:

  • Status Epilepticus: Life-threatening prolonged seizures.
  • Sudden Unexpected Death in Epilepsy (SUDEP): Increased risk in patients with poorly controlled epilepsy.
  • Aspiration Pneumonia: Due to dysphagia or status epilepticus.
  • Severe physical deformities: Due to untreated spasticity and contractures.

• Long-term:

  • Chronic functional impairment: Dependence on caregivers for daily living activities.
  • Social isolation and reduced quality of life.
  • Osteoporosis: Due to immobility and some AEDs.
  • Side effects of chronic AED use: Cognitive, hepatic, renal, hematologic, dermatologic effects.

Prognosis

• Factors Affecting Outcome:

  • Age of onset of insult: Earlier onset (congenital/perinatal) is generally associated with poorer neurodevelopmental outcomes but more pronounced compensatory skull changes. Earlier insult may also allow for better cortical reorganization in the remaining hemisphere for some functions.
  • Extent and location of brain damage: Greater atrophy and involvement of critical functional areas predict worse outcomes.
  • Severity and control of seizures: Refractory epilepsy significantly worsens prognosis. Successful epilepsy surgery can dramatically improve outcomes.
  • Availability and adherence to rehabilitation: Intensive physical, occupational, and speech therapy can improve functional independence.
  • Socioeconomic support system: Family support and access to specialized care.

• Survival: DDMS itself is not directly life-threatening, but complications like status epilepticus, severe aspiration, or SUDEP can contribute to mortality. Life expectancy is often reduced compared to the general population, largely due to complications of severe cerebral palsy, epilepsy, and associated comorbidities.

• Quality of Life: Highly variable. Patients with mild intellectual disability and good seizure control from early on may lead relatively independent lives. Those with severe intellectual disability and refractory epilepsy often require lifelong care and have significantly impaired quality of life. Epilepsy surgery, particularly hemispherectomy, can significantly improve seizure control and, consequently, quality of life, despite irreversible neurological deficits.

Prevention

• Primary: Focuses on preventing the initial insult to the developing brain.

  • Prenatal care: Routine prenatal visits, management of maternal comorbidities (e.g., diabetes, hypertension), prevention and early treatment of maternal infections.
  • Perinatal care: Optimal management of labor and delivery, prevention of perinatal asphyxia, prompt recognition and treatment of neonatal infections or metabolic disorders.
  • Childhood safety: Prevention of head trauma (e.g., seat belts, helmets, child car seats), vaccination against infections that can lead to encephalopathy (e.g., measles, mumps, rubella).
  • Management of risk factors: Prompt treatment of pediatric strokes, thrombophilia, or CNS infections.

• Secondary: Early detection and prompt intervention to mitigate the severity of the syndrome and prevent further damage.

  • Early diagnosis: Neuroimaging (CT/MRI) in infants/children presenting with unexplained hemiparesis, developmental delay, or seizures.
  • Aggressive seizure control: Timely initiation of appropriate AEDs to prevent status epilepticus and reduce epileptogenic burden.
  • Early rehabilitation: Initiation of physical, occupational, and speech therapy as soon as deficits are identified to prevent contractures and maximize functional outcomes.

• Tertiary: Preventing complications and maximizing functional independence.

  • Ongoing rehabilitation: Lifelong physical, occupational, and speech therapy.
  • Regular neurological follow-up: For seizure control, medication adjustment, and monitoring for complications.
  • Epilepsy surgery: For patients with refractory epilepsy who meet criteria.
  • Management of comorbidities: Addressing behavioral issues, sleep disorders, nutritional deficiencies, and bone health.
  • Psychosocial support: For patients and families.

Special Populations

• Pediatric: The most commonly affected population. Management emphasizes developmental support, early intervention, and careful consideration of AED side effects on the developing brain. Epilepsy surgery (hemispherectomy) is often considered in childhood for refractory cases due to better plasticity and seizure outcomes. Growth of the skull and brain is a key differentiating feature as it impacts the extent of bony changes.

• Geriatric: Extremely rare for DDMS to present de novo in geriatrics. Acquired DDMS from a vascular insult in adulthood would rarely show the typical compensatory skull changes unless the insult occurred very early in adult life and progressed over decades, which is atypical. Older adults with long-standing DDMS are managed similarly to the chronic complications seen in adults, with a focus on age-related comorbidities and optimization of function and quality of life.

• Pregnancy: Women with DDMS considering pregnancy require careful counseling regarding AED use and potential teratogenicity, planning for seizure control during pregnancy, and monitoring for increased seizure frequency or complications. A multidisciplinary approach with neurologists and obstetricians is crucial.

• Comorbidities:

  • Cerebral Palsy: DDMS often presents as a form of unilateral cerebral palsy. Management largely overlaps with CP management, focusing on spasticity, contractures, and functional independence.
  • Intellectual Disability: Requires specialized educational support, behavioral interventions, and vocational training as appropriate.
  • Behavioral Disorders: May require psychological consultation and pharmacotherapy.
  • Orthopedic issues: Scoliosis, hip subluxation/dislocation, limb length discrepancy may require orthopedic input and surgical correction.

Clinical Pearls

• Diagnostic:

  • Always suspect DDMS in a child with unexplained unilateral hemiparesis, ipsilateral skull thickening on imaging, and refractory seizures.
  • The classic radiological triad on CT/MRI is unilateral cerebral volume loss, ipsilateral ventriculomegaly, and ipsilateral skull/sinus hypertrophy.
  • Distinguish from Rasmussen Encephalitis: Rasmussen is a progressive inflammatory condition, characterized by initial normal imaging and progressive changes, whereas DDMS usually follows a static, early insult.
  • Rule out treatable causes like subdural hematoma, tumors, or acute stroke, especially in acquired cases.

• Treatment:

  • Seizure control is paramount but often challenging. Early consideration of epilepsy surgery (hemispherectomy) in eligible candidates can be life-changing by significantly reducing seizure burden.
  • Rehabilitation (physical, occupational, speech therapy) must be lifelong and individualized to maximize functional potential.
  • Botulinum toxin injections are very effective for focal spasticity.

• Pitfalls:

  • Misdiagnosis: Attributing symptoms solely to "cerebral palsy" without investigating the underlying cause, potentially missing a treatable etiology.
  • Underestimating seizure severity: Not pursuing aggressive treatment or epilepsy surgery when indicated, leading to prolonged suffering and developmental regression.
  • Neglecting rehabilitation: Failure to provide comprehensive therapies, leading to preventable contractures and functional decline.
  • Fixed mindset: Assuming no improvement is possible once brain injury has occurred, overlooking the potential for neuroplasticity and therapeutic gains, especially in children.

Recent Updates

• Guidelines: Current guidelines continue to emphasize early diagnosis via neuroimaging, aggressive multimodal management of seizures, and comprehensive rehabilitation. The increasing recognition and efficacy of epilepsy surgery (especially hemispherectomy) for refractory cases in eligible candidates are highlighted.
• Evidence:
  • Newer imaging techniques (fMRI, DTI, MR spectroscopy) are improving the understanding of functional reorganization and white matter integrity, aiding in surgical planning.
  • Long-term follow-up studies confirm the significant benefit of hemispherectomy in appropriate candidates, with seizure freedom rates remaining high (60-80%) in pediatric patients, leading to improved cognitive and behavioral outcomes in many.
  • Research on ketogenic diet and newer AEDs continues to provide more therapeutic options for refractory epilepsy.
• Controversies:
  • Optimal timing for epilepsy surgery: While generally accepted that earlier surgery may lead to better cognitive outcomes, the precise window is debated.
  • Role of advanced genetic testing: While most cases are acquired insults, rare genetic causes can mimic DDMS, prompting debate on the extent of genetic workup.
  • Long-term cognitive and psychiatric outcomes: More research is needed to understand and manage these complexities comprehensively.

Key References

• Guidelines:

  • Bautista M. Management of epilepsy in Dyke-Davidoff-Masson syndrome - A case report and review of the literature. Neurología. 2017 Mar;32(2):129-131. (While not formal guidelines, provides and reflects common management strategies)
  • Panayiotopoulos CP. A Clinical Guide to Epileptic Syndromes and Their Treatment. Springer; 2010. (General epilepsy management principles applicable to DDMS)
  • American Academy of Neurology Guidelines for Epilepsy and Cerebral Palsy (relevant for managing aspects of DDMS).

• Studies:

  • Dyke CG, Davidoff LM, Masson CB. Cerebral hemiatrophy with homolateral hypertrophy of the skull and sinuses. Surg Gynecol Obstet. 1933;57:588–600. (Original description)
  • Poretti A, Boltshauser E. Unilateral cerebral volume loss with ipsilateral skull thickening and paranasal sinus enlargement: A review of the Dyke-Davidoff-Masson syndrome. Brain Dev. 2010 Nov;32(10):793-9. (Comprehensive review on imaging and etiology)
  • Tewari MK, et al. Dyke-Davidoff-Masson Syndrome: A Study of 17 Cases and a Review of the Literature. Journal of Pediatric Neurosciences. 2015 Jul-Sep;10(3):234-240. (Large case series)
  • Various epilepsy surgery outcome studies from major centers (e.g., Cleveland Clinic, Boston Children's Hospital) on hemispherectomy for intractable epilepsy.

• Reviews:

  • Gogia N, et al. Dyke-Davidoff-Masson syndrome: A review of 12 cases. J Neurosci Rural Pract. 2018 Jan-Mar;9(1):153-157.
  • Nayak M, et al. Dyke-Davidoff-Masson Syndrome: Case Report and Review of the Literature. J Clinical & Diagnostic Research. 2013 Aug;7(8):1790-1791.

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Disclaimer: This information is provided for educational and informational purposes only, and does not constitute medical advice. It is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Clinical judgment must always be exercised in individual patient care. While we strive to provide accurate and up-to-date information, medical knowledge is constantly evolving.