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  2. 2.  Paraplegia is the word comes from Greek language para + plēssein. means ‘strike at side’  Paraplegia is defined as impairment in motor function of the lower extremities with or without involvement of sensory system  It is usually caused by involvement of cerebral cortex, spinal cord, the nerves supplying the muscles of lower limbs or due to involvement of the muscles directly
  3. 3. Complete paralysis is paraplegia where as partial paralysis is known as paraparesis paraplegia is of two types (Depending upon the part of nervous system involved and resulting tone)spastic paraplegia and flaccid paraplegia.
  4. 4. SPASTIC PARAPLEGIA  weakness of muscles along with increased tone  it occurs in UMN diseases due to loss of inhibition of contraction  increased muscle tone, exaggerated deep tendon reflexes, planter extension with or without clonus.  Further it is divided in 2 types paraplegia in extension and paraplegia in flexion
  5. 5.  paraplegia in extension :-  Occurs In initial stages or partial transaction of spinal cord with  involvement of pyramidal tract,  hypertonia is more in extensor group of muscles  paraplegia in flexion :-  occurs as the disease or lesion progresses further or with complete transaction of spinal cord  extra pyramidal tracts get involved leas to  more hypertonia in flexor group of muscles resulting in flexed posture of limbs.
  6. 6. Paraplegia in extension Paraplegia in flexion 1. Cause Pyramidal lesion Pyramidal and extrapyramidal eeeeextraextrapyramidapyramidalexpyramidal 2. Hypertonia More in extensors More in flexors 3. Position of L.L Extended Flexed 4. Deep reflexes Exaggerated Less exaggerated 5. Clonus Present Absent 6. Mass reflex Absent May be present 7. Bladder Precipitancy Automatic bladder
  7. 7. FLACCID PARAPLEGIA  decreased tone and contractility of muscles along with weakness.  it occurs in lower motor neuron diseases  due to loss of stimulatory innervation to muscle.  decreased muscle tone, atrophied muscle, absent deep tendon reflexes, flexor or equivocal planters with or without fasciculations
  8. 8. CAUSE OF PARAPLEGIA  1.Cerebral:- A. Causes in the Parasagittal Region:  1. Traumatic e.g. depressed fracture of the vault of the skull, Subdural hematoma.  2. Vascular e.g. superior sagittal sinus thrombosis.  3. Inflammatory e.g. encephalitis, meningio-encephalitis.  4. Neoplastic e.g. parasagittal meningioma.  5. Degenerative e.g. cerebral palsy.  B. Causes in the Brain Stem:  Syringobulbia and midline tumors. These lesions arise in the midline and involve the innermost fibers which are those of the lower limbs
  9. 9.  2. Spinal  1. intramedullary:- Syringomyelia, hematomyelia, ependymoma, glioma, astrocytoma  2.Extramedullary :-  2a:-intradural:- meningioma, neurofibroma, arachnoiditis  2b:-Extradural:-  vertebral:- Fracture or fracture-dislocation of the vertebra, Disc prolapse and spondylosis, Deformity of the vertebral (e.g. kyphoscoliosis)  infective:- Pott's disease,  congenital:-spina bifida,  Neoplastic diseases:-Primary(myeloma) or metastatic(leukemia),  Paravertebral:-abscess, hematoma, aortic aneurysm
  10. 10.  3.Infective Causes: Bacterial: Acute: Staphylococcal (extradural or intradural) Chronic: Tuberculous, Syphilitic.  Parasitic: Hydatid, cysticercosis, Schistosomiasis.  Viral: Polio, Rabies, Herpes zoster, HIV  4.Inflammatory: Transverse myelitis - Myelomeningitis - Myeloradiculitis.  5.Immuno Allergic causes:  Post vaccinial-Rabies, tetanus, and polio Post exanthematous- Chicken pox, Herpes zoster  6.Demyelinating:  Multiple sclerosis, Neuromyelitis optica, Sub acute combined degeneration
  11. 11.  7.Heredo familial, Degenerative: Spinocerebellar degeneration. Herditory spastic paraplegia, Hereditary ataxias e.g. Friedreich's or Marie's ataxia, Motor neuron Disease  8.Toxic myelopathy: Lathyrism, Arsenic, Contrast media used in radiology, Intra thecal penicillin, Spinal anesthesia, peripheral neuropathy.  9.Vascular Disorder: Arteriosclerosis- Anterior spinal artery thrombosis  Dissecting aneurysm of aorta, AV malformation in spinal cord  10.Metabolic /Nutritional; B12 deficiency. Pellagra, Myelopathy of chronic liver disease  11.Tropical; Tropical spastic paraplegia  12.Para Neoplastic Syndromes  13.Physical agents;_ Irradiation, Electric shock to spinal cord
  12. 12.  Normal motor function depending upon segmental spinal cord level  C1-C6:- Neck flexors C1-T1:-neck extensors  C3-C5:- supply diaphragm (mostly c4)  C5-C6:- shoulder movement, raise arm(deltoid) flexion of elbows(biceps)  C6:- externally rotates the arm(supinator)  C6-C7:- extends elbow and wrist (triceps and wrist extensor), pronates arm  C7-T1:- flexes wrist  C7-T1:- supply small muscles of hand
  13. 13.  T1-T6:- intercostal muscles  T7-L1:- abdominal muscles  L1-L4:- thigh flexion  L2-L4:- thigh adduction  L4-S1:- thigh abduction  L5-S2:- extension of leg at hip (gluteus maximus)  L2-L4:- extension of legs at knee(quad. femoris)  L4-S2:- flexion of leg at knee (hamstrings)  L4-S1:- dorsiflexion of foot  L5-S2:- planter flexion of foot  L4-S1:- extension of toes  L5-S2:- flexion of toes
  14. 14. CLINICAL FEATURES:-  In addition to weakness of lower limbs other clinical features depends on the cause of paraplegia  In cerebral paraplegia there may be weakness of upper limbs also along with other features i.e.- mental retardation, delayed milestones, siezures, altered sensorium. etc.  In Spinal paraplegia there is spasticity, exaggerated DTR, radicular pain, dermatomal sensory involvement with specific motor weakness depending upon level of spine affected  Distal weakness, sensory loss, muscle atrophy, absent tendon reflexes favours peripheral nerve involvement
  15. 15. APPROACH TO PATIENT :-  History:- ask about onset :-sudden (Trauma-fracture dislocation of vertebrae Infection: Epidural Abscess, Vascular: Thrombosis of ASA Endarteritis , Hematomyelia. Transverse Myelitis Gradual ( Neoplastic- meningioma, ependymoma, glioma, astrocytoma etc.)  Duration of symptoms(short duration in traumatic, infective causes and long duration in neoplastic, hereditary, congenital, demyelinating causes etc. )  Sensory :- Ask about pattern of sensory loss i.e. sacral sparing or sacral area involved. Radicular (root) pain indicates an extradural lesion,  Whether the limb involvement is symmetrical or serial, whether weakness is more in proximal muscles or distal, whether weakness is progressive or static
  16. 16.  Associated symptoms (fever: infective causes. seizures, delayed milestones: cerebral cause. And associated various specific systemic symptoms e.g. vitamin deficiency etc.)  Proper history should be asked about any preceding illness, specific trauma, prior vaccination, involuntary movements  Ask about bladder and bowel involvment  In younger children it is important to ask about antenatal, natal and post natal history(maternal infection, perinatal asphyxia, hyperbilirubinemia, hospitalization etc)  Ask about significant past history and family history
  17. 17.  Examination:-  complete systemic examination including proper neurological examination is must  It includes; higher mental function status(affected in cerebral and degenerative diseases)  cranial nerve examination(affected in brain stem leisons)  Tone(increased in UMN and decreased in LMN disease)  DTR(exaggerated in UMN leisons and absent in LMN leisons and spinal shock)
  18. 18.  Sensory examination (to asses particular sensory level and to what extent and which sensation is lost)  Proper examination of skull and spine (to look for any localized tenderness, depressed fracture, deformity etc.)
  19. 19. Features Intramedullary Intradural extramedullary Extradural extramedullary Involvement Usually asymmetrical Asymmetrical Usually symmetrical Progression Slow Usually slow Rapid Root pain Rare Less common More common Fasciculations Not uncommon Rare rare Trophic skin changes Present Rare Uncommon Muscle atrophy Wide due to ant. Horn cell involvement Wide involvement if anterior cells are involved One or two segments at the site of root involvement Spasticity Less common May be present Common
  20. 20. Position sense Spared Lost if posterior column is involved Lost early Pain and temp sensation Lost early Lost if spinothalamic tract involved Lost late Dissociative sensory loss Present Absent Absent Bladder and bowel involvement Early Late Late Spinal tenderness Rare Less common Common CSF Normal May be abnormal Frequently abnormal X ray spine(bony changes) Absent May be present Present
  21. 21.  Some specific signs and symptoms which helps in evaluating the level of spinal cord involvement  Upper cervical region& foramen magnum:  Severe pain in the occiput &neck.  In hands loss of post. column sensation is early symptom & severe tingling & numbness.  Pain & weakness in the limbs & wasting may occur in the upper limb.  Decreased diaphragm Movements due to compression of phrenic nerve.  Lower cranial nerve involvement & medullary involvement can occur.  Descending tract of trigeminal can be involved.
  22. 22.  C5C6 segment lesion:  inverted supinator reflex  wasting of muscles supplied by C5C6 namely deltoid, biceps, brachioradialis, rhomboids,  Paraplegia  C8T1 Level:  Wasting of small muscle of hands.  Wasting of flexors of wrist & fingers. Horner’s syndrome.  DTR of upper limbs preserved.  Spastic paralysis of trunk & lower limbs.  Cervical spondylosis never involves C8&T1 so small muscle wasting rules out cervical spondylosis.
  23. 23.  Mid Thoracic region of spinal cord:  Upper limb normal.  Wasting of intercostal muscles (those supplied by involved segments)  Movements of diaphragm normal.  Spastic paralysis of abdominal muscles &lower limbs.  9th &10th thoracic segments:  Lower abdominal muscles are weaker and upper abdominal muscles are intact  BEEVOR’S SIGN positive (when patient raises the head against resistance umbilicus is drawn upwards).
  24. 24.  T12L1 segments:  Abdominal reflexes preserved  Cremastric reflex lost.  Wasting of internal oblique & transverse abdominal muscle  L3 L4 segmental lesion:  Flexion of hip is preserved. Cremastric reflex preserved.  Quadriceps & adductors of hip are wasted  knee jerk is lost or diminished. But ankle jerk is present  Plantar-extensor. Foot drop
  25. 25.  S1S2 segments;  Wasting & paralysis of intrinsic muscles of feet.  Wasting & paralysis of calf muscles Plantor flexion impaired.  But dorsi flexion of foot is preserved.  In the hip all muscles of hip are preserved except flexors & adductors.  In the knee flexors of knee are wasted.  KNEE JERK IS PRESERVED, ANKLE JERK IS LOST.  Plantar reflex is lost. No foot drop.  Anal & Bulbocavernous reflexes are preserved.
  26. 26.  S3S4 segments:  Large bowel & bladder are paralysed.  There is retension of urine and feces due to unopposed action of internal sphincters.  The external sphincters are paralyzed.  Anal and bulbo cavernous reflex are lost  Saddle shaped anasthesia occurs. but no paraplegia
  27. 27.  CALCULATING SEGMENTS INVOLVED FROM VERTEBRAL LEVEL  For upper cervical vertebrae same level  For lower cervical vertebra Add1  For T1-T6 – vertebrae Add2  ForT6-T9- vertebrae Add3  T10 vertebra corresponds to L1L2 segments  T11 vertebra corresponds to L3L4 segments  T12 vertebra corresponds to L5 segment  L1 vertebra overlies Sacral and coccygeal segments
  28. 28. INVESTIGATIONS  Routine blood tests (HB, TC, DC, GBP) Blood chemistry (eg. blood urea, creatinine, electrolytes etc.)  Routine urine exam,urine for culture and sensitivity  Plain Xray Spine (Lateral and oblique view):  reduction in vertebral ht with irregularity of the antero-superior end plate and irregularity of the ant. vertebral margin (pott’s spine)  Reduction of iv space, Narrowing of iv foramina (spinal cord trauma, disc prolapse)  Osteophyte formation, Widening of IV foramina (Neuro fibroma)  Destructed or collapsed of vertebra (Secondaries, myeloma, TB infection)  pedicle erosion (extra medullary tumor)  Para spinal mass(extra medullary tumor /cold abscess).
  29. 29.  CSF Analysis;  R/M:-s/o infection-bacterial/tubercular/viral meningitis  In spinal cause CSF protein is often increased especially below the block, more so in extra medullary leisons  CSF:- culture and sensitivity testing  C.S.F.-Electrophoresis to show oligoclonal bands of multiple sclerosis  L. P. can worsen neurological disease, because of the pressure gradient it creates. So when a compressive lesion is suspected LP & CSF analysis can be done at the time of Myelography..
  30. 30.  CT scan:  CT cranium :-Plain CT it can diagnose acute intracranial bleed and fracture of skull bone, and contrast CT can show f/o ischemic changes, infective lesion, degenerative, and neoplastic leisons   Spinal CT :- plain CT Can diagnose narrowing of disc space, disease of lumbar region. Can identify narrowing of lumbar canal & thickening of facet joint.  Contrast CT is required to show Cord compression. Can show amount of compression & delineate neurofibroma like intraspinal lesions
  31. 31.  MRI:  MRI brain is more informative than CT. it helps in diagonosing, degenerative, neoplastic, vascular and infective leisons.  Spinal MRI usually Saggital views are taken Can differentiate Syringomyelia from intramedullary tumors, transverse myelitis etc.  It also shows cord compression whether internal or external
  32. 32.  Myelogram  A. Extradural:  Complete block:- shows ragged edge. At times even with complete block contrast can be coaxed beyond the block to determine its upper extent otherwise a cervical puncture may be required.  In Partial block:- Dura mater is lifted away from the vertebral body.  B. Intra dural  Intra medullary; contrast is splayed around dilated cord.  Extramedullary; cord displaced to one side.
  33. 33. COMPRESSIVE MYELOPATHY  Clinical features depends on part of spinal cord got involved  Spinal nerve roots:- dorsal nerve root involvement produce u/l or b/l pain aggravated by sudden rapid body movement where as ventral nerve root involvement produce LMN type of paraperesis  Corticospinal tract:- usually this structure is involved early  Produce weakness(assymetrical) and stiffness of lower limbs  Posterior column:- produce loss of position, vibration and sense of passive movements with girdle like sensation
  34. 34.  Spinothalamic tract:- produce parasethesia i.e. numbness, coldness  further compression results in impairment of pain and temp. sensation of other half of body  Vessel compression:- venous compression cause edema of cord below the level of lesion an produce symptoms at lower level,  arterial compression cause ischemia of segment of cord and produce symptomps at and below the level of lesion
  35. 35. SYRINGOMYLEIA  cystic dilatation of the spinal cord caused by the obliteration of the flow of CSF from within spinal canal to its point of absorption.  It is of 3 type  1.communicating syringomylia  2.non-communicating   Has insidious course from years to decades .  produces central cord syndrome  tropic ulcers are common in advanced cases .  Urgency and bladder dysfunction with lower extremity spasticity may be a part of presentation
  36. 36.  MRI with contrast is the radiological study of choice .  Treatment should be tailored to the underlying cause.  drainage procedures can result in symptomatic and radiographic improvement.  syrinx to subarachnoid shunting, syrinx to plueral or syrinx to peritoneal shunting
  37. 37. HEMATOMYELIA  Hemorrhage into the substance into spinal cord occurs due to trauma, vascular malformations, bleeding disorders or spinal cord neoplasms .  Presents as an acute transverse myelopathy ,  diagnosed by MRI or CT .  Therapy is supportive  surgical intervention is generally not required except in vascular malformations .
  38. 38. EPIDURAL ABSCESS  it can form anywhere along spinal canal.  two thirds of epidural abscess results from hematogenous spread of infection and one third from direct extension of local infections.  Risk factors are—impaired immune status and nearby infections of the soft tissue.  It presents with triad of pain, fever and rapidly progressive weakness.  Treatment-is emergency decompressive laminectomy with debridemnt or drainage of abscess with long term antibiotics.
  39. 39. POTT’S DISEASE  Also known as spinal TB or tubercular spondylitis  infection reaches by hematogenous spread in most cases and in small no. of cases from adjacent paravertebral lymph nodes  It often involves two or more vertebral bodies.  upper thoracic spine is the most common site for spinal TB.  From one vertebral body lesion slowly reaches the adjacent vertebral body later affecting the intervertebral disc.
  40. 40.  paravertebral cold abscess can also be formed .  collapsed vertebra or abscess cause compression of the spinal cord leading to paraparesis or paralysis in severe cases  x ray spine shows decreased vertebral height collapsed vertebrae and irregular vertebral margins .  CT and MRI spine reveals characteristic lesions .  Treatment is drainage of abscess if present, start ATT with steroids and spinal support
  41. 41. ANTERIOR SPINAL ARTERY INFRACTION  It supplies the ant. two thirds of the spinal cord ,  its infarction causes anterior cord syndrome :-paraplegia or quadriplegia, dissociated sensory loss affecting pain and temp sensation but sparing vibration and position sense and loss of sphincter control.  Course may be sudden or gradual depending upon the cause .  sharp midline or radiating back pain, localized to the area of ischemia is common complain.
  42. 42.  Areflexia present initially (due to spinal shock) followed by hypereflexia and spasticity  Causes are- aortic atherosclerosis, dissecting aortic aneurysm, vertebral artery block, cardiac emboli, profound hypotension.  Acute anticoagulation is not indicated in presented thromboembolism.  Drainage of spinal fluid has been reported successful in some cases.
  43. 43. AV MALFORMATION OF SPINAL CORD  most often located posteriorly within dura or along the surface of cord at or below mid thoracic level.  rare cases but important because they represent treatable causes of progressive myelopathy.  patient has motor, sensory and bladder disturbances along with intermittent claudication and effect of posture, menses or fever on symptoms.  Vascular lesion of overlying skin, lipoma or area of altered pigmentation given clue for diagnosis.  bruit are rare but should be sought at rest or after exercise
  44. 44.  MRI with contrast detects most of the AVM.  definitive diagnosis requires selective spinal angiography which may also detect feeder and extent of malformation .  Embolization with occlusion of major feeding vessels may stabilize progressive neurological deficit or produce a gradual recovery.  open microsurgery has been the mainstay of the treatment .  stereotactic radiosurgery may be used urgently
  45. 45. HEREDITARY SPASTIC PARAPLEGIA:-  Familial Spastic Paraplegias, French Settlement Disease, or Strumpell-Lorrain Disease  It may be inherited as AD, AR, or X-linked disease. Most common is AD (70% to 80%)  characterized by progressive lower limb spasticity secondary to pyramidal tract dysfunction.  results in brisk DTR, extensor planters, muscle weakness, abnormal gait and variable bladder disturbances.  HSP are often mistakenly diagnosed as cerebral palsy  It is classified as pure if neurologic signs are limited to the lower limbs
  46. 46.  In contrast, complicated forms of HSP display additional neurologic and MRI abnormalities such as ataxia, peripheral neuropathy, mental retardation, or a thin corpus callosum  In children with spastic paraplegia in whom no acquired cause can be identified, HSP should be considered.  Diagnosis of HSPs relies upon family history, the presence or absence of additional signs and the exclusion of other nongenetic causes of spasticity  confirmation of HSP can only be provided by carrying out genetic tests targeted towards known genetic mutations
  47. 47. SUBACUTE COMBINED DEGENERATION  due to vitamin B12 deficiency & involves post column.  Present as early loss of vibration and position sense with parasthesia of hands and feet and progressive spastic and ataxic weakness ,  loss of reflexes due to superimposed peripheral neuropathy is important clue to diagnosis.  Advanced cases may present with optic atrophy , irritability and mental changes .  myelopathy is generally diffused and symmetrical.  Diagnosis is by low vitamin B 12 levels with increased homocysteine methylmalonic acid and positive schilling test.
  48. 48. FRIEDREICH’S ATAXIA  AR, mutation is in mitochondrial protein frataxin,  it leads to oxidative injury a/w excessive iron deposit in mitochondria  can involve spinocerebellar tract , dorsal column, pyramidal tract, cerebellum or medulla.  Ataxia is slowly progressive and involves lower extremity more than upper limbs.  o/e rhomberg test is positive with absent DTR and extensor planters with characterstic explosive disarthric speech and nystagmus .
  49. 49.  also charaterised by skeletal abnormalities hammer toes and progressive kyphoscoliosis.  Hypertrophic cardiomyopathy with progression to intractable CHF is the cause of death.  visual evoked response, BERA and somatosensory evoked potentials are abnormal.  Antioxidant therapy, with coenzyme q-10 and vitamin E had been reported to slow progression in some cases.
  50. 50. HYDROCEPHALUS  dilatation of cerebral ventricles and increase CSF pressure .  it may be congenital or acquired.  acquiductal stenosis is the most common cause of congenital hydrocephalus.  among acquired causes -intraventricular haemorrhage, malignancy, infections are common causes.  Vomiting ,dizziness, failure to thrive, delayed milestones.  ocular signs are 6th nerve palsy ,sunset sign, ptosis and nystagmus may be present.
  51. 51.  spasticity of lower limb occurs due to compression of periventricular white matter.  pseudobulbar palsy may be present.  CT or MRI with or without contrast will assess the degree of ventricular dilatation and possible etiology.  Goal of therapy is decreasing intracranial pressure (hypertonic saline, acetazolamide, furosemide) &  maximizing the potential for neurological development by preserving brain parenchymal thickness.  Surgical treatment options are VP shunt and endoscopic third ventriculostomy.
  52. 52. PARASAGITTAL MENINGIOMA:-  term applies to those tumors involving the sagittal sinus and the adjacent convexity dura and falx.  Only the lateral wall of the sinus may be involved or the tumor may grow to partially or completely occlude the sinus  tumors arising from the middle third of the sagittal sinus and falx are the most common  They present with focal motor or sensory symptoms or gradual loss of neurological function usually begins in the lower extremity.
  53. 53.  Tumors arising from the ant. Third have a insidious onset and often become large before a diagnosis is made.  There may be a gradual change in personality, progressive dementia, apathy and Seizures & Headache  Tumor arising from the post. third presents with headache or other symptoms and signs of raised ICP  MRI outlines the tumor and may indicate the status of the sagittal sinus.  Angiography is usually needed to assess the status of the sinus and the relationship of cortical veins.  Management is gross total resection
  54. 54. GUILLAIN BARRE SYNDROME  immune mediated, rapidly progressive, predominantly motor symmetrical polyradiculoneuropathy  multiple types such as AIDP, acute motor axonal neuropathy, mixed, acute motor and sensory neuropathy, acute pandysautonomia and miller fisher syndrome  Acute onset symmetrical ascending weakness of both proximal and distal muscle.  facial weakness is common and respiratory involvement occurs in one fourth cases.  weakness usually reaches nadir in 2 to 4 weeks after onset of symptoms followed by gradual recovery over wks to months
  55. 55.  Dysautonomia is common and is suggested by tachycardia , arrhythmia , labile BP ,bladder dysfunction and impaired thermoregulation  Diagnosis depends on clinical features, electrophysiology(NCV) - absent f wave ,reduced compound muscle action potential (in axonal form)  prolonged distal latencies, reduced conduction velocities and conduction block (in demyelinating form)  Albumino cytological dissociation is found in CSF(usually after 7 days of illness)
  56. 56. TRANSVERSE MYELITIS  rapid development of both motor and sensory deficits.  occurs in two distinct contexts  1.less than 3 years of age , rapid course over hrs to days with history of infectious disease (viral),immunization within few weeks preceding the illness.  Recovery is slow and likely to be incomplete.  pathological finding of perivascular infiltration with mononuclear cells implies an infectious or inflammatory basis.  2.more than 3 years of age –onset is relatively slow with nadir in neurological functions between 2 days to 2 weeks.
  57. 57.  recovery is rapid and likely to be complete.  pathological or imaging examination shows acute demyelination  neck and back pain and progress to numbness, sensory level and weakness in trunk and limbs .  paralysis begins as flaccidity but over a few weeks spasticity develops ,urinary retention is early finding  MRI with contrast helps in diagnosis and also rules out other mass lesions .  in CSF presence of inflammatory cells are essential for diagnosis of transverse myelitis  Modulation of immune response may be effective in decreasing the severity and duration of illness
  58. 58. MANAGEMENT OF PARAPLEGIA  I. General:  Frequent change of the patient's posture to guard against bedsores.  Care of the skin by frequent washing with alcohol followed by talc powder. In case of urinary incontinence, frequent change of bed-sheets.  Care of the bladder: If there is retention, use parasympathomimetic drugs. If this fails, use a catheter to evacuate the bladder.  II. Physiotherapy
  59. 59.  III. Symptomatic Treatment:  Analgesics and sedatives for pain, Muscle relaxants for the spasticity, Vitamins and mineral supplementation.  IV.Specific Treatment: (treatment of the cause)  Eg. Antituberculous drugs along with supportive measures in Pott's disease.  Drainage of paraspinal abscess, traumatic spine stabilisation  Surgical management of some tumors.  Deep X—ray in case of intramedullary tumors, etc.  v. rehabilitation: it includes management of complications, occupational therapy, gait retaining and community re- integration
  60. 60. COMPLICATIONS OF PARAPLEGIA  Bed sores  Contractures  Urinary tract infection  Pneumonia  Deep venous thrombosis
  61. 61. REFRENCES  Nelson’s text book of pediatrics 19th edition.  Harrison’s principle of internal medicine 17th edition.  Adam and victor text book of neurology  Manual of pediatric neurology  Ghai essential pediatrics 8th edition.  Piyush gupta text book of pediatrics 1st edition.