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Spina bifida

Spina bifida






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    Spina bifida  Spina bifida Presentation Transcript

    • Neural groove- dorsum of embryoDeepens- FurrowCloses- Neural canalCENTRAL NERVOUS SYSTEM4thweek of IUL
    •  Lumen persists as – Central neural canal. Closure◦ Starts in cervical region◦ Proceeds caudally & cranially◦ Cranium closing last – 26 days Neural tube◦ Proliferating cells of neuroepithelium differentiate –NEUROBLASTS or NEURONS. Motor axons – out growing processes. Sensory neurons – from neural crests (Ectoderm & Postsurface of neural tube).
    •  Meninges – arise from loose mesenchymaltissue surrounding the N. tube.◦ Pia mater – 40 days◦ Dura – later. Neural canal separates from ectodermalcovering – ingrowth of mesoderm. Notochord –◦ solid rod of cells◦ Anterior to N. canal Vertebral bodies develop around this all.
    •  From each of the Vertebral bodies◦ Extend backwards 2 projections◦ Grow around N. canal◦ Form – Vertebral arch◦ Fuse behind thoracic region – extend up & down.
    •  FUSION FAILS – Gap in vertebral N arch SPINA BIFIDA◦ m.c. in Lumbosacral region
    •  Latin word for “split spine”. Literally means “cleft spine,” Most common group of birth defects called neuraltube defects (NTD). Incidence◦ World wide about 1 per 1000 live births.
    •  Antenatal screening of AFP - 15–18 mths.◦ Identify at risk women.◦ If high AFP – Amniocentesis and USG. Previous neural tube defect fetus –◦ 10 fold increased risk◦ 50 fold for third pregnancy. Genetic predisposition. Some environmental factors
    •  The exact cause of spina bifida remains amystery.  Genetic, nutritional, and environmentalfactors may play a role.  Combination of genetic and environmental riskfactors, such as a family history of neural tubedefects, folic acid deficiency and medicalconditions such as diabetes and obesity.
    •  Race: more common among Hispanics andwhites of European descent. Family history of neural tube defects.However, most babies with spina bifida are bornto parents with no known family history of thecondition.
    •  Folic acid deficiency (vitamin B-9)increases the risk of spina bifida and otherneural tube defects.◦ MRC recommend F. acid supplimentation for high riskmothers. Some medications. Anti-seizure medications,such as valproic acid, seem to cause neuraltube defects when taken during pregnancy,perhaps because they interfere with the bodysability to use folic acid.
    •  Diabetes: Especially when the mothers bloodsugar is elevated early in her pregnancy. Muchof this risk is preventable by careful blood sugarcontrol and management. Obesity. Theres a link between pre-pregnancyobesity and neural tube birth defects, includingspina bifida. Obese women may have morebabies with spina bifida possibly because ofnutritional deficits from poor eating habits orbecause they may have diabetes.
    •  Increased body temperature. Some evidencesuggests that increased body temperature(hyperthermia) in the early months of pregnancymay increase the risk of spina bifida. Contaminated potatoes – blamed in humans. Experimental defects – Vit A def., Azodyes, X rays& disturbed Zn metabolism.
    •  Von Recklinghausen 1886◦ Due to failure of the posterior mass of neural tube.
    •  Two headings:1. Spina bifida cystica1. Meningocele2. Myelomeningocele3. Syringomyelocele4. Myelocele5. Anterior spina bifida2. Spina bifida occulta
    •  Saccular trusion ofonly meninges Pia & Arachnoid Dura stops at bonymargins Spinal cord is not involved No paralysis Sac contains only CSF
    •  5 % of Spina bifida cystica. Surgical closure required – to prevent rupture andmeningitis. Associated lesions◦ Lipomata◦ Cyst formation◦ Dilation of spinal canal – hydromyelin.
    •  Majority of SBC Gap in spinal columnthrough which protrudes1. Flat plaque of N. tissue.2. Meninges surrounding it. Spinal cord – open on theback surface for 3-4segments.
    •  Plaque and meninges – enlarge to sac –increasing CSF within few hours of birth. Sac – burst – during or just after birth. CSF leak – infection. 3 Zones on surface:1. Central neural plaque (Vasculosa)2. The meninges (Serosa)3. Surrounding hairy & thickened skin (Dermatica)
    •  Spinal cord is spread out to form lining of the sac& is thinned into a cyst by distension of centralcanal of the cord.
    •  Myelocele:◦ Gross spinal cord deformity◦ Elongated fissure surrounded by telangiectases or hair –in direct contact with central canal.◦ m.c. in lumbosacral region. Anterior Spina Bifida◦ Very rare – anterior defect.
    •  Often unnoticed Incidentally on radiograph. Spinal cord and meninges normal One or more bony arches are incompletely closedposteriorly. Dura may be attached to skin – fibrous band –MEMBRANA REUNIENS
    •  Lipomata or Angiomata – in or outside thevertebral canal. Hairy patch – overlying skin. Membrana reuniens doesn’t elongate with growth– traction lesion of cord – praralytic deformity of Llimbs or bladder.
    •  Called by Till - Occult spinal dysraphism:1. Diplomyelia2. Diastematomyelia3. Others – Intraspinal lipomata or hydromyelia of centralcanal. Urinary incontinence, neurological abnormalities(esp in L limbs) or meningitis by infected dermalsinus. Need Radiography, myelography or MRI beforesurgery.
    •  The American Academy of OrthopaedicSurgeons Committee for the Care of theHandicapped Child (1974)1. Open defects:1. Myelomeningocele (Hydromyelia, dysraphismrachischisis)2. Meningocele3. Dermal sinus.
    •  Closed defects:1. Spina bifida occulta:1. Diastematomyelia2. Intraspinal tumor (Lipoma, chondroangioma,dermoid).2. Myelodysplasia:1. Aplasia or hypoplasia of nerve roots or cord.2. Absent anterior horn cells (Arthrogryposis)3. Diplomyelia (Double cord)
    • 3. Errors in skeletal segmentation:1. Absence of sacrum2. Absent lumbar vertebrae3. Hemivertebrae4. Congenital segmental fusion5. Failure of fusion or absent odontoid process6. Others.
    •  Stark & Baker (1967) – two main types:◦ TYPE-I (~33%) – Complete loss of all spinal cord funtionbelow the lesion level – flaccid paralysis, sensorydeficiency & absent reflexes.◦ TYPE-II (~66%) – Preservation of reflex activities fromintact distal segment but interruption corticospinal tractswith paralysis. Three subgroups depending on severity.
    •  Early operation at 48 hrs. without selection – Initialoptimism – by Sharrard◦ Survival rate improved◦ Quality of life – pitiful.
    •  Lorber 1971 defined factors associated with badprognosis – used as basis for selection:◦ Gross paralysis in TLS region.◦ Esp with scoliosis or kyphosis◦ Enlarging hydrocephalus◦ Intracerebral injury◦ Heart abnormality◦ Meningitis or gross mental disturbance.
    •  Principles of combined management – bySharrard et. al in Sheffield – directed to 5 majorproblems:1. Myelomeningocele2. Hydrocephalus3. Urinary tract paralysis4. Locomotor system5. Education
    •  To achieve INDEPENDENCE asfar as possible. Role of Orthopaedic surgeon –provide – by surgical or nonsurgical means, the ability to sitand stand as well as effective butnot excessive demandingwalking.
    •  Surgical closure of myelomeningocele – wheneverindicated – within 48hrs. Baseline neurological examination, headcircumference & assessment of any hipdislocation. Hydrocephalus drained from dilated lateralventricle.
    • Thank You!