1. PARAPLEGIA
DR. NAVEEN KUMAR IMS BHU VARANASI

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. 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. 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.  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. 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. 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. 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

10.  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

11.  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

12.  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

13.  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

14.  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

16. 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

17. 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

18.  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

19.  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)

20.  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.)

21. 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

22. 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

23.  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.

24.  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.

25.  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).

26.  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

27.  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.

28.  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

29.  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

30. 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).

31.  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..

32.  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

33.  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

34.  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.

35. 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

36.  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

37. 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
 3.post-traumatic
 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

38.  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

40. 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 .

41. 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.

43. 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.

44.  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

46. 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.

47.  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.

48. 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

49.  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

51. 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

52.  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

53. 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.

54. 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 .

55.  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.

56. 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.

57.  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.

58. 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.

59.  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

60. 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

61.  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)

62. 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.

63.  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

64. 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

65.  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

66. COMPLICATIONS OF PARAPLEGIA
 Bed sores
 Contractures
 Urinary tract infection
 Pneumonia
 Deep venous thrombosis

67. 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.