Mass reflex In severe injury of spinal cord, stimulation below the level of the lesion produces flexion reflexes of the lower limb, evacuation of bowel and bladder and sweating of the skin below the level of the lesion.
Intradural- assymmetrical involvment with slow progression
Horner syn. Ptosis miosis, anhidrosis enapthalmos due to sympethetic syst involvement
Cs tract involved early it is supplied by terminal branch of ant spinal artery and lies close to ligamentum denticulum
Cnt. Cord synd-more extensive motor weakness in the upper extremities than the lower extremities because in corticospinal tract arm fibers medially, and the leg fibers laterally
A hammer toe is a deformity of the proximal interphalangeal joint of the second, third, or fourth toe causing it to be permanently bent, resembling a hammer. Mallet toe is a similar condition affecting the distal interphalangeal joint
CSF inflammatory cells are essential for diagnosis of transverse myelitis (nelson)
Transcript of "Paraplegia"
DR. NAVEEN KUMAR IMS BHU VARANASI
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
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
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.
weakness of muscles along with increased tone
it occurs in UMN diseases due to loss of inhibition
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
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.
Paraplegia in extension Paraplegia in flexion
1. Cause Pyramidal lesion Pyramidal and extrapyramidal
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
decreased tone and contractility of muscles along
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
CAUSE OF PARAPLEGIA
1.Cerebral:- A. Causes in the Parasagittal Region:
1. Traumatic e.g. depressed fracture of the vault of the skull,
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
1. intramedullary:- Syringomyelia, hematomyelia,
ependymoma, glioma, astrocytoma
2a:-intradural:- meningioma, neurofibroma, arachnoiditis
vertebral:- Fracture or fracture-dislocation of the vertebra, Disc
prolapse and spondylosis, Deformity of the vertebral (e.g.
infective:- Pott's disease,
Neoplastic diseases:-Primary(myeloma) or
Paravertebral:-abscess, hematoma, aortic aneurysm
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 -
5.Immuno Allergic causes:
Post vaccinial-Rabies, tetanus, and polio Post exanthematous-
Chicken pox, Herpes zoster
Multiple sclerosis, Neuromyelitis optica, Sub acute combined
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
9.Vascular Disorder: Arteriosclerosis- Anterior spinal artery
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
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
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
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
APPROACH TO PATIENT :-
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,
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
Whether the limb involvement is symmetrical or serial, whether
weakness is more in proximal muscles or distal, whether weakness is
progressive or static
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
complete systemic examination including proper neurological
examination is must
It includes; higher mental function status(affected in cerebral and
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
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.)
Features Intramedullary Intradural
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
Wide involvement if
anterior cells are
One or two segments at
the site of root
Spasticity Less common May be present Common
Position sense Spared Lost if posterior column
Pain and temp sensation Lost early Lost if spinothalamic
Dissociative sensory loss Present Absent Absent
Bladder and bowel
Early Late Late
Spinal tenderness Rare Less common Common
CSF Normal May be abnormal Frequently abnormal
X ray spine(bony
Absent May be present Present
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 &
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.
C5C6 segment lesion:
inverted supinator reflex
wasting of muscles supplied by C5C6 namely deltoid, biceps,
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.
Mid Thoracic region of spinal cord:
Upper limb normal.
Wasting of intercostal muscles (those supplied by involved
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).
Abdominal reflexes preserved
Cremastric reflex lost.
Wasting of internal oblique & transverse abdominal
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
Wasting & paralysis of intrinsic muscles of feet.
Wasting & paralysis of calf muscles Plantor flexion
But dorsi flexion of foot is preserved.
In the hip all muscles of hip are preserved except flexors
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.
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
CALCULATING SEGMENTS INVOLVED FROM
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
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
Reduction of iv space, Narrowing of iv foramina (spinal cord
trauma, disc prolapse)
Osteophyte formation, Widening of IV foramina (Neuro
Destructed or collapsed of vertebra (Secondaries, myeloma,
pedicle erosion (extra medullary tumor)
Para spinal mass(extra medullary tumor /cold abscess).
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
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..
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
MRI brain is more informative than CT. it helps in
diagonosing, degenerative, neoplastic, vascular and
Spinal MRI usually Saggital views are taken Can
differentiate Syringomyelia from intramedullary tumors,
transverse myelitis etc.
It also shows cord compression whether internal or
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
B. Intra dural
Intra medullary; contrast is splayed around dilated cord.
Extramedullary; cord displaced to one side.
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
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
Spinothalamic tract:- produce parasethesia i.e.
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
arterial compression cause ischemia of segment of cord
and produce symptomps at and below the level of lesion
cystic dilatation of the spinal cord caused by the obliteration of
the flow of CSF from within spinal canal to its point of
It is of 3 type
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
MRI with contrast is the radiological study of choice
Treatment should be tailored to the underlying
drainage procedures can result in symptomatic and
syrinx to subarachnoid shunting, syrinx to plueral or
syrinx to peritoneal shunting
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 .
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
Risk factors are—impaired immune status and nearby
infections of the soft tissue.
It presents with triad of pain, fever and rapidly progressive
Treatment-is emergency decompressive laminectomy with
debridemnt or drainage of abscess with long term antibiotics.
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
From one vertebral body lesion slowly reaches the
adjacent vertebral body later affecting the intervertebral
paravertebral cold abscess can also be formed .
collapsed vertebra or abscess cause compression of the
spinal cord leading to paraparesis or paralysis in severe
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
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
sharp midline or radiating back pain, localized to the area
of ischemia is common complain.
Areflexia present initially (due to spinal shock) followed
by hypereflexia and spasticity
Causes are- aortic atherosclerosis, dissecting aortic
aneurysm, vertebral artery block, cardiac emboli,
Acute anticoagulation is not indicated in presented
Drainage of spinal fluid has been reported successful in
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
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
open microsurgery has been the mainstay of the
stereotactic radiosurgery may be used urgently
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
In contrast, complicated forms of HSP display additional
neurologic and MRI abnormalities such as ataxia,
peripheral neuropathy, mental retardation, or a thin
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
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.
AR, mutation is in mitochondrial protein frataxin,
it leads to oxidative injury a/w excessive iron deposit in
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 .
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.
dilatation of cerebral ventricles and increase CSF
it may be congenital or acquired.
acquiductal stenosis is the most common cause of
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.
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
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.
Tumors arising from the ant. Third have a insidious
onset and often become large before a diagnosis is
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
GUILLAIN BARRE SYNDROME
immune mediated, rapidly progressive, predominantly motor
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
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)
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
2.more than 3 years of age –onset is relatively slow with
nadir in neurological functions between 2 days to 2
recovery is rapid and likely to be complete.
pathological or imaging examination shows acute
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
MANAGEMENT OF PARAPLEGIA
Frequent change of the patient's posture to guard against
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.
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
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-
COMPLICATIONS OF PARAPLEGIA
Urinary tract infection
Deep venous thrombosis
Nelson’s text book of pediatrics 19th edition.
Harrison’s principle of internal medicine 17th
Adam and victor text book of neurology
Manual of pediatric neurology
Ghai essential pediatrics 8th edition.
Piyush gupta text book of pediatrics 1st edition.