Spinal Cord Injury (SCI) PDF - Introduction and Neuroanatomy

Spinal Cord Injury (SCI) Introduction and Neuroanatomy Dr. Manjiri Dahdul PT, DPT  Objectives I. Describe the differences and similarities between UMN and LMN spinal cord lesions. II. Describe the clinical presentation of most common SCI syndromes. III. R...

Spinal Cord Injury (SCI) Introduction and Neuroanatomy Dr. Manjiri Dahdul PT, DPT  Objectives I. Describe the differences and similarities between UMN and LMN spinal cord lesions. II. Describe the clinical presentation of most common SCI syndromes. III. Recognize the key signs and symptoms of autonomic dysreflexia (AD). IV. Determine the sensory and motor neurological levels in a patient with SCI based on the ASIA scale. V. Distinguish between bowel and bladder issues with UMN and LMN spinal cord lesions.  Neuroanatomy Neuroanatomy Pathogenesis General considerations Step 1 Pathogenesis General Disease course Clinical findings Clinical findings Disease course Red flags Step 2 Diagnosis Diagnosis/differential diagnosis Medical management Medical management Clinical management Prognosis Step 3 Clinical management Prognosis  CNS vs. PNS CNS PNS Neuroanatomy UMN Sensory Other LMN Sensory Autonomic Motor CN and Cranial nerves: Cortical Cortical Basal ganglia nuclei* sensory and special Cerebellum Anterior horn* Spinal peripheral Brainstem Brainstem nerve and nerve root Cortical Spinal nerve root association areas and peripheral Spinal Spinal nerve cord (e.g., cognition, cord behavior) NMJ Autonomic: hypothalamus, basal ganglia, Muscle limbic system, brainstem, spinal cord *Nuclei are in the CNS; but are the start of the LMN  General Considerations Spinal cord ends Spinal Nerves Neuroanatomy C1 C2 C3 Cervical cord L1–L2 (UMN) C4 C5 C6 C7 C8 Conus medullaris T1 T2 T3 T4 Thoracic T5 cord Cauda equina T6 T7 T8 T9 T10 L2 and below (LMN) T11 T12 Lumbar cord L1 Sacral cord Coccygeal cord L2 Clinical L3 relevance L4 Cauda L5 equina ? S1 S2 S3 Timmons L and Raia N. S4 S5 Treating spinal cord injuries with Co1 Filum terminale stem cells  Transverse Section of Spinal Cord Bone Spur Neuroanatomy Prevertebral plexus Prevertebral ganglion (sympathetic) Aorta Vertebral body Anterior root Sympathetic ganglion Visceral components Anterior ramus Picture credit: Posterior ramus http://drwolgin.com/laminoplasty/ Posterior root Spinal nerve Burst Fracture Lamina Extradural space Arachnoid mater Spinal cord Dura mater Pia mater Subarachnoid space Spinous process Picture credit: https://www.mbbsinchina.com Picture credit: http://www.radiopaedia.org  UMN vs. LMN UMN: lateral cortical spinal Neuroanatomy tract (in spinal cord) LMN: anterior horn cell and spinal nerve root Martin. Neuroanatomy Text and Atlas. 4th ed. McGraw Hill; 2011.  Case Video SCI video-unit3 copy.mp4  Tracts of the Spinal Cord UMN and LMN! Neuroanatomy Gracile fascicle Medial vestibulospinal tract Cuneate fascicle Lateral corticospinal tract Dorsal spinocerebellar tract Rubrospinal tract Anterior horn cell Tectospinal tract Ventral Medullary spinocerebellar reticulospinal tract tract Anterolateral Ventral corticospinal tract Pontine system reticulospinal Lateral tract vestibulospinal tract Adapted from: Martin. Neuroanatomy Text and Atlas, 4th ed. McGraw Hill, 2011.  Spinal Cord Syndromes Medial Gracile vestibulospinal Lateral cord Cuneate fascicle fascicle tract Lateral corticospinal (Brown-Séquard)* Dorsal tract Clinical Management spinocerebellar tract Rubrospinal Complete cord Anterior tract Tectospinal Central cord horn cell tract Ventral Medullary Anterior cord spinocerebellar tract reticulospinal tract Posterior cord Anterolater Ventral corticospinal Pontine al system tract reticulospinal Pure motor Lateral tract vestibulospinal tract Conus Cauda equina Martin. Neuroanatomy Text and Atlas, 4th ed. McGraw Hill; 2011.  Spinal Cord Syndromes Clinical Management Blumenfeld. Neuroanatomy Through Clinical Cases. 2nd ed. Sinauer Associates, Inc.; 2002.  Clinical Findings Initial spinal shock Clinical Findings Blumenfeld. Neuroanatomy Through Clinical Cases. 2nd ed. Sinauer Associates, Inc. 2002.  Prevalence/Incidence General Considerations In an instant…your life could change drastically… Between 8000 and 50,000 acute SCI injuries in North America each year* About 305,000 people living in the U.S. (2023) Most common causes: MVA > falls > violence 60% children or young adults ≤ 30 years * Typically 16–30 years Mean age: 42.0 years (2017) Men affected 4x > women (80.9%) Get Out Your Licorice!  Traumatic SCI Etiology Initial injury via four different mechanisms I. Impact with persistent compression Etiolgoy (burst fracture) II. Impact with transient compression post hyper/injuries III. Distraction: forcible stretching of spinal cord or blood supply IV. Laceration from missile injury, sharp bone fragment dislocation, or severe distraction Pathogenesis Rodriguez et al. The metabolic response to spinal cord injury. Spinal Cord. September 1997;35(9):599–604. Pathogenesis Spinal cord axons Macrophages Glial Scar Picture credit: https://repositorio-aberto.up.pt/bitstream  Neuroinflammation and Recovery Microenvironment is critical Pathogenesis Inflammation at the lesion site is well-known, however less known at different levels inflammation may occur 10 segments away Potential to improve recovery with inflammation Inflammation (specifically in the L/S) can produce: I. Maladaptive neuroplasticity II. No motor learning  Disease Course Disease Course Acute onset, then progressive to stable Spinal shock Stable with flaccid Emergency Neurologic return Initial paralysis, response Possible UMN Most recovery: one traumatic loss of Immobilization signs year sensation, and stabilization *Spasticity Most rapid recovery: event and motor Diagnosis via MRI first six months *Hyperreflexia function  Diagnostic Studies MRI *diagnostic tool of choice X-rays Diagnosis CT EMG NCV  Medical Management Standard of care Experimental Immobilization: halo, TLSO Implanted spinal stimulators Medical Management *avoid prolonged Locomotor training immobilization Nanofibers aka “Dancing Early intervention: closed Molecules” reduction, spinal decompression Corticosteroids: early Methylprednisolone IV bolus BP management General care Nutritional support  Prognosis Mortality post-SCI 4–17% Predisposing factors: age, higher levels, pulmonary embolism, medical co-morbidities, and suicide Predictive factors for recovery potential Prognosis (Table 14-12) Brown-Séquard syndrome greatest potential for recovery (75–90% walk independently post DC/70%ADLs) Central cord syndrome: lower extremity (LE) recovery, bowel and bladder function seen early Age: < 50: faster, more successful recovery Ability to attain intensive locomotor training  Issues in Rehab of Spinal Cord Injury Clinical Management Bladder Bowel Decubitus Autonomic Dysfunction Dysfunction Ulcers Dysfunction Sexual Wheelchair Spasticity Dysfunction seating & positioning  UMN lesion (C1-L1 ) LMN lesion (L2-S5 ) Bowel Hyperreflexic (spastic paralysis) Areflexic (flaccid paralysis) *Reflex is intact *No tone is muscles Bladder Spastic (urinary bladder and Areflexic (detrusor is unable to sphincter are overactive) contract) Symptoms Bowel: constipation, difficulty Bowel: constipation, difficulty Clinical Management with evacuation and with evacuation and incontinence, AD incontinence Bladder: increased Bladder: retention/failure to frequency of urination/failure empty urine to store urine *Possible damage to kidneys and Inability to fully empty the bladder wall bladder Clinical Bowel: reflex defecation; stool Bowel: stool softener, minimal management softener, laxative and strain to void suppository or rectal stim Bladder: catheterization, Bladder: catheterization, prevention of urinary tract prevention of urinary tract complications, and complications, and pharmacologic management pharmacologic management *Consistent bowel program is critical *Distinction between UMN and LMN depends on the segmental levels affected vs. vertebral levels  Autonomic Dysreflexia Exaggerated, massive autonomic response to strong sensory stimuli Clinical Management Loss of inhibitory control of sympathetic neurons Generally lesions T6 and above Common causes: bladder and bowel distension, ulcers, constrictive clothing, ingrown toenails Remove strong stimuli Medical emergency! RED FLAG! *Monitor vitals, check common noxious stimuli, do not lay supine  Sympathetic Parasympathetic nervous nervous system system Eye Oculomotor nerve (III) Facial nerve (VII) Lacrimal and salivary glands Clinical Management Glossopharyngeal nerve (IX) Superior cervical ganglion Lung Cervical Stellate ganglion Heart Vagus nerve (X) Celiac ganglion Thoracic Liver Stomach Pancreas Adrenal medulla Small intestine Lumbar Large intestine, Superior rectum mesenteric ganglion Sacral Inferior mesenteric Bladder Sympathetic ganglion trunk Reproductive organs Adapted from: Martin. Neuroanatomy Text and Atlas. 4th ed. McGraw Hill; 2011.  Fig 1: Diagram illustrating how autonomic dysreflexia occurs in a person with spinal cord injury 6. Baroreceptors in blood vessels detect hypertensive Brain crisis - signal brain Carotid and aortic 7a. Heart rate IX, X slowed baroreceptors X C D Vagus nerve 7b. Descending inhibitory Spinal cord signals blocked at spinal (CN X) cord injury Heart 5. Hypertension Level of spinal cord injury = T6 or above Spinal cord injury Sympathetic outflow 4. Widespread vasoconstriction Diaphragm B BP 3. Massive A sympathetic Splanchnic response Skin breakdown blood vessels 2. Afferent stimulus Full bladder Fecal impaction 1, Full bladder or stimulus from bowel Blackmer J CMAJ 2003;169:931-935 ©2003 by Canadian Medical Association  Autonomic Dysreflexia Pounding headache Flushed (reddened) (caused by in BP) face Clinical Management Hypertension (BP > Nausea 200/100) Slow pulse Diaphoresis above (< 60 beats/minute) the level of injury Cold, clammy skin Red blotches on the below the level of the skin above level of spinal injury spinal injury Restlessness Cutis anserina Nasal congestion (goose bumps)  Sexual Dysfunction: Males Autonomic nervous system essential to penile erection Parasympathetic nervous system: Clinical Management initiates erectile response (S2–4) Sympathetic nervous system: ejaculation (L1–3) Most common issues Erectile dysfunction (ED) Ejaculation Fertility Treatment options for ED: Surgical procedures (penile prosthesis) Vacuum devices Pharmacology  Sexual Dysfunction: Females Autonomic nervous system T11–L2: innervates uterus Clinical Management S1–S4: innervates vulva and vagina Most common issues Altered menstrual period Lubrication Hormonal changes Fertility—often not affected  Spasticity Velocity-dependent increase in tonic stretch reflexes with passive Clinical Management movement UMN: lesions above cauda equina Initially absent immediately post acute injury—develops over weeks Stretching/contracture management Medications: Baclofen, Tizanidine, Diazepam, Dantrolene, and Clonodine Botox, Xeomin, phenol nerve blocks Intrathecal baclofen pump  American Spinal Injury Association (ASIA) Clinical Management Picture credit: https://asia-spinalinjury.org  ASIA Impairment Scale A: Complete—no motor or sensory function is preserved in the sacral segments S4–5 Clinical Management B: Incomplete—sensory but not motor function is preserved below the neurological level and includes the sacral segments S4–5 C: Incomplete—motor function is preserved below the neurological level, and more than half of the key muscles below the neurological level have a muscle grade less than 3 D: Incomplete—motor function is preserved below the neurological level, and at least half of the key muscles below the neurological level have a muscle grade of 3 or more E: normal—motor and sensory functions are normal  ASIA Neurological Levels How to determine sensory/motor and neurological level? Sensory level: the most caudal level normally innervated dermatome for both pin prick and light touch (grade 2) **Right vs. left may differ Motor level: the most caudal level, normal or intact innervated spinal nerve In regions where there is not a myotome to be tested (thoracic spine), the motor level is presumed to be the same as the sensory level **Must be a grade ≥ 3, provided the next most rostral key muscle tests as normal (grade 5) Neurologic level: the most caudal segment of the cord where sensory and motor is intact  L2 Hip L3 flexors Quads L4 Tibialis anterior L5 Picture credit: https://asia-spinalinjury.org The motor level is the most caudal level with a grade of at least 3, as long as the more rostral levels are normal (5).  Steps in Classification The following order is recommended for determining the classification of individuals with SCI. 1. Determine sensory levels for right and left sides. The sensory level is the most caudal, intact dermatome for both pin prick and light touch sensation. 2. Determine motor levels for right and left sides. Defined by the lowest key muscle function that has a grade of at least 3 (on supine testing), providing the key muscle functions represented by segments above that level are judged to be intact (graded as a 5). Note: In regions where there is no myotome to test, the motor level is presumed to be the same as the sensory level, if testable motor function above that level is also normal. Picture credit: https://asia-spinalinjury.org  Steps in Classification The following order is recommended for determining the classification of individuals with SCI. 3. Determine the neurological level of injury (NLI). This refers to the most caudal segment of the cord with intact sensation and antigravity (3 or more) muscle function strength, provided that there is normal (intact) sensory and motor function rostrally respectively. The NLI is the most cephalad of the sensory and motor levels determined in steps 1 and 2. 4. Determine whether the injury is Complete or Incomplete. (i.e. absence or presence of sacral sparing) If voluntary anal contraction = No AND all S4-5 sensory scores = 0 AND deep anal pressure = No, then injury is Complete. Otherwise, injury is Incomplete. Picture credit: https://asia-spinalinjury.org  Steps in Classification The following order is recommended for determining the classification of individuals with SCI. 5. Determine ASIA Impairment Scale (AIS) Grade. Is injury Complete? If YES, AIS = A NO Is injury Motor Complete? If YES, AIS = B NO (No=voluntary anal contraction OR motor function more than three levels below the motor level on a given side, if the patient has sensory incomplete classification) Are at least half (half or more) of the key muscles below the neurological level of injury graded 3 or better? NO YES AIS=C AIS=D If sensation and motor function is normal in all segments, AIS = E Note: AlS E is used in follow-up testing when an individual with a documented SCI has recovered normal function. If at initial testing no deficits are found, the Individual is neurologically intact and the ASIA Impairment Scale does not apply. Picture credit: https://asia-spinalinjury.org  Nontraumatic Disorders of the Spinal Cord Syringomyelia Diagnosis Spina bifida Myelitis Spinal epi/subdural SC infarction hematoma Spinal epidural abscess  Syringomyelia Fluid-filled gliosis-lined cavity starts in central canal Irregular cavity Etiology unclear Disrupts central structures and anterior horn of gray matter Diagnosis Associated with spinal column or brainstem abnormalities (scoliosis, Klippel-Feil syndrome, Arnold Chiari malformation) Third and fourth decades of life *typical **Can begin in childhood Diagnostic studies: MRI and CT C2 and T9–11 spinal levels Picture credit: https://pediatricneurosurgery.org/si tes/default/files/syrinx-mri.jpg  Syringomyelia Diagnosis Picture credit: https://www.brighton.ac.uk  Syringomyelia Gracile fascicle Medial vestibulospinal tract Cuneate fascicle Lateral corticospinal tract Loss of pain Dorsal Segmental Clinical Findings spinocerebellar and tract atrophy Rubrospinal temperature tract Anterior horn cell Tectospin al tract Ventral Medullary spinocerebellar tract reticulospina Proprioception l tract Areflexia intact Anterolateral Ventral corticospinal tract Pontine system reticulospinal Lateral tract vestibulospinal tract Progression: a. Long motor tracts affected b. Sensory tracts affected (UE > LE) Post-traumatic Syringomyelia: a. Symptoms above or below the original injury b. Worsening pain or neurological function Martin. Neuroanatomy Text and Atlas, 4th ed. McGraw Hill; 2011.  Syringomyelia Conservative Medical Management I. Avoid high-force isometric contractions II. Avoid Valsalva expiration III. Head elevation at night IV. Maintain neutral neck Surgical interventions I. Decompression II. Shunt replacement III. Tumor resection and radiation (intramedullary spinal cord tumors)  Spina Bifida Spina Myelomeningocele bifida aperta Diagnosis Spina bifida Aperta: visible Meningocele or open Birth defect Incomplete closure Spine and membranes Spina bifida Most common occulta Occulta: hidden Often or not visible asymptomatic  Types of Spina Bifida Spina bifida aperta: myelomeningocle Spina bifida Dura mater Subarachnoid space Arachnoid Diagnosis Spinal cord Myelomeningocele Meningocele Spina bifida occulta Spina bifida occulta Meningocele Meningomyelocele Picture credit: https://www.kfshrc.edu Sullivan RD. The relationship between ventriculoperitoneal shunts and shunt revisions versus visual complaints among patients with spina bifida in the Arkansas spina bifida research project. 2012.  Spina Bifida Aperta Myelomeningocele (MMC): The most severe form of spina bifida Diagnosis Protrusion of the spinal meninges and spinal cord through a defect in the vertebral column Open spinal cord defect, not Picture credit: https://bettercare.co.za/learn/congenital- skin covered disorders/text/10-photographs.html Usually associated with nerve paralysis…but not always  Myelomeningocele (MM) Diagnosis Picture credit: https://bettercare.co.za/learn/congenital-disorders/text/10-photographs.html  Clinical Findings The degree of motor and/or sensory loss varies Clinical Findings Musculoskeletal deformities High risk: I. Neurogenic bowel and bladder, UTIs, latex allergies II. Arnold Chiari type II,hydrocephalus No two patients are clinically identical High risk for loss of function over time  Surgical and Medical Management Surgical closure of myelomeningocele Surgical correction of orthopedic deformities Medical Management Placement of ventriculoperitoneal (VP) shunt Medications for the management of bowel and bladder function Fetal meningomyelocele repair Picture credit: Picture credit: https://www.childrens.health.qld.gov.au https://www.midwestcompassion.org  Prognosis Despite surgery, affected nerves may still not function normally Typically normal intelligence Due to risk of hydrocephalus and meningitis; Learning problems Seizure disorders Prognosis Spinal cord issues can develop later in life Rapid growth during puberty ↑ risk of progressive neurological impairments Orthopedic problems (scoliosis, foot or ankle deformities, dislocated hips, and joint tightness or contractures. Three most common complications leading to decline in function: 1. Syringomyelia Public Service Announcement: folic acid 2. Tethered spinal cord deficiency is associated with ↑ risk of SB. So taking prenatal vitamins is important if 3. Shunt dysfunction you think you are pregnant or could get pregnant!  Hydrocephalus Definition: excessive accumulation of cerebrospinal fluid in the ventricles of the brain 25% of children with MMC are born with hydrocephalus 60% develop it after the Picture credit: radiopaedia.org surgical closure of their back lesion  Hydrocephalus Age Physical symptoms Physical signs Behavioral/cognitive change Infants Vomiting, sleepiness, Unusually large head irritability, poor Rapid ↑ in the size of feeding, seizures, the head abnormal muscle Bulging soft spot tone Toddlers/ Headaches, blurred Abnormal enlargement of Irritability, change in school-aged vision the head circumference, personality, attention children sleepiness, nausea deficit, decline in vomiting, unstable school performance, balance, poor loss of skills (motor, coordination UE and LE; language) poor appetite; seizures Adults Headaches, lethargy, Loss of coordination or Decline in memory, blurred vision balance, loss of bladder impaired control concentration, decline in job performance  Hydrocephalus 80–90% of children with hydrocephalus require a CSF shunt Ventriculoperitoneal catheter shunt (VP shunt) Left untreated, can cause severe cognitive impairments Occasionally resolves spontaneously Picture credit: https://www.midwestcompassion.org  Ventriculoperitoneal (VP) Shunt Relieves pressure from the brain caused by fluid accumulation Primarily used to treat hydrocephalus Surgically placed inside ventricles to divert fluid away from the brain Picture credit: https://www.midwestcompassion.org Ventriculoperitoneal (VP) Shunt Likely to require replacement after several years Infants: last for two years on average Children two years and older: can last upwards of 10 years Common complications associated with the shunt system: Mechanical failure Obstruction Infection Catheter may need to be lengthened or replaced Shunt malfunction can lead to over- or under draining of the CSF  VP Shunt Malfunction Shunt malfunction signs: Headaches Vomiting Lethargy Irritability Swelling or redness along the shunt tract Decreased school performance Confusion Seizures Diagnosis: CT or MRI to confirm growth of ventricles Shunt tap: Test pressure along catheter Test CSF for infection Arnold Chiari Malformation, Syrinx, and Tethered Cord Dr. Manjiri Dahdul PT, DPT  Arnold Chiari II Malformation Tissue from the cerebellum, medulla, and fourth ventricle become displaced into the foramen magnum. Almost all children with MMC have an Arnold Chiari II malformation. The malformation interferes with the normal flow of the CSF Picture credit: radiopaedia.org around the brain and spinal cord. It leads to a buildup of fluid in the ventricles of the brain, leading to hydrocephalus.  Arnold Chiari II Malformation Type II Chiari malformation is specifically in 4th ventricle patients with spina bifida; often accompanied Bra instem by a syrinx Cerebellum Always involves displacement of the C1 Tonsil cerebellum and brainstem C2 C1 Foramen Spinal cord magnum Change in the morphology of the medulla and C2 pons (elongated), narrowed aqueduct, and possibly bony abnormalities of the skull including small posterior fossa, foramen magnum misshaped, base of the skull flattened Typically diagnosed at birth or during infancy after the diagnosis of spina bifida; diagnosed via ultrasound or CT scan Symptoms include changes in breathing pattern, swallowing problems, gagging, quick downward eye movements, weakness in the upper extremities  Syringomyelia Fluid-filled gliosis-lined cavity starts in central canal Irregular cavity Etiology unclear Disrupts central structures and anterior horn of gray matter Diagnosis Associated with spinal column or brainstem abnormalities (scoliosis, Klippel-Feil syndrome, Arnold Chiari malformation) Third and fourth decades of life *typical **Can begin in childhood Diagnostic studies: MRI and CT C2 and T9–11 spinal levels Picture credit: https://pediatricneurosurgery.org/si tes/default/files/syrinx-mri.jpg  Syringomyelia Gracile fascicle Medial vestibulospinal tract Cuneate fascicle Lateral corticospinal tract Loss of pain Dorsal Segmental Clinical Findings spinocerebellar and tract atrophy Rubrospinal temperature tract Anterior horn cell Tectospin al tract Ventral Medullary spinocerebellar tract reticulospina Proprioception l tract Areflexia intact Anterolateral Ventral corticospinal tract Pontine system reticulospinal Lateral tract vestibulospinal tract Progression: a. Long motor tracts affected b. Sensory tracts affected (UE > LE) Post-traumatic Syringomyelia: a. Symptoms above or below the original injury b. Worsening pain or neurological function Martin. Neuroanatomy Text and Atlas, 4th ed. McGraw Hill; 2011.  Tethered Cord Occurs from scarring of the spinal cord or meninges to the overlying dura or skin Resultant traction on neural structures Detected via MRI Fatty tissue may tether the filum 20–50% of children with Normal Tethered cord spina bifida defects Thickened filum repaired shortly after birth will require surgery at some Picture credit: http://www.brainandspinesurgeryli.co point in their lifetime to m untether their spinal cord  Tethered Cord Signs and symptoms: Deterioration of “normal” gait pattern Loss of sensation Loss of strength Pain along a dermatome Initial onset or worsening of Picture credit: spasticity https://radiopaedia.org Change in bowel/bladder sphincter control  Key Concepts I. The spinal cord ends between L1–L2 vertebrae (UMN) II. The cauda equina is a collection of nerve roots that begins at the end of the spinal cord and exits from the third lumbar vertebra to the fifth sacral vertebra (LMN) III. Compare and contrast the most common SCI syndromes IV. AD is an exaggerated autonomic response to a strong sensory stimuli that is a medical emergency typically for SCI levels T6 and above V. Sensory and motor levels definitions: ASIA classification VI. Differences and similarities between bowel and bladder dysfunction  UMN (C1–L1) LMN (L2–S5) Syringomyelia Myelomeningocele Trauma Trauma Nontraumatic Developmental Etiology Spasticity and mild Atrophy Segmental atrophy Motor and sensory loss Signs/ atrophy (disuse) Weakness Areflexia varies Symptoms Weakness Areflexia Pin prick impaired Musculoskeletal Hyperreflexia Vibration intact deformities MRI MRI MRI MRI Diagnostic CT CT CT CT Tests X-ray Varies depending on Varies depending on Varies depending ↑risk of progressive Prognosis/ predictive factors predictive factors on: neurological Progression (Brust, table 14-12) (Brust, table 14-12) Classification impairments Expansion Varies depending on: Treatment The extent of damage The level of defect Surgical interventions Therapeutic interventions Immobilization Immobilization Conservative Surgical closure of Treatment myelomeningocele Surgical intervention Surgical intervention Surgical Surgical correction of Corticosteroids and Corticosteroids and decompression orthopedic deformities neuroprotective neuroprotective Placement of VP shunt strategies strategies Medications: bowel and BP management BP management bladder management General care General care Fetal meningomyelocele repair *Surgical intervention *Distinction between UMN and LMN depends on the segmental levels affected vs. vertebral levels Thank You!