PARA PLEGIAS

DR.PRAVEEN NAGULA

PARAPLEGIAS

Important terms PARALYSIS – loss of power of voluntary movements in a muscle

through injury or disease of it or its nerve supply.

PARAPLEGIA – paralysis of both lower extremities.

QUADRIPLEGIA – paralysis of all four limbs.

HEMIPLEGIA –paralysis of one side of the body.

CROSSED HEMIPLEGIA – hemiplegia on one side with C/L cranial nerve palsies.

ANESTHESIA – absent perception of all sensations , mainly touch.

PARESTHESIAS – spontaneous abnormal sensations that is not unpleasant.

DYSESTHESIAS –unpleasant abnormal sensation described by the patient.

HYPERPATHIA – abnormally painful and exaggerated reaction to a painful stimulus.

HYPERALGESIA – extreme sensitivity to painful stimulus.

ALLODYNIA –pain perception with non painful stimulus.

SPINAL CORD ANATOMY Thin tubular extension of the CNS contained within the bony

spinal canal.

It originates at the medulla and continues caudally to the conus medullaris at the lumbar level.

Filum terminale is the fibrous extension of the cord terminates at the coccyx.

It is 46 cm in length ,oval in shape

Cervical and lumbar enlargements –neurons innervating upper limb and lower limb are located.

Inner gray matter outer white matter

Ascending sensory and descending motor tracts are located peripherally.

Gray matter containing the nerve cell bodies –four leaf clove shape

Surrounds a central canal –extension of fourth ventricle.

VERTEBRAL

COLUMN

CENTRAL

NERVOUS

SYSTEM

Conus medullaris

Cauda equina

The cross sectionOf

Spinal cordWith

meningeal sheaths

Tracts in the spinal cord

Cont…

Spinal cord has 31 segments.

Each spinal segment has a pair of EXITING ventral motor roots and ENTERING dorsal sensory roots.

Growth of spinal cord lags behind the vertebral column and spinal cord ends at approximately the first lumbar vertebral body.

Lower spinal nerves take an increasingly downward course to exit via intervertebral foramen.

SPINAL CORD LEVELS RELATIVE TO THE VERTEBRAL BODIES

EX- C4 lesion –C4, C8—C7 T5 --- T3 T12– T9 L3—T12 S3 – L1

SPINAL CORD LEVEL CORRESPONDING VERTEBRAL BODY

UPPER CERVICAL 4 SEGMENTS

SAME AS CORD LEVEL

LOWER CERVICAL 1 LEVEL HIGHER

UPPER THORACIC 6 SEGMENTS

2 LEVELS HIGHER

LOWER THORACIC 2-3 LEVELS HIGHER

LUMBAR T10-T12

SACRAL T12-L1

DETERMINING THE LEVEL OF LESION

The presence of a horizontally defined level below which sensory , motor and autonomic function is impaired is a hallmark of spinal cord disease

Sensory level Identify the pin prick or cold stimulus applied to

the proximal legs and lower trunk subesequently moving up towards the neck on each side.

Sensory loss below the level is as a result of damage to the SPINOTHALAMIC TRACT on the OPPOSITE SIDE one to two segments higher in case of a unilateral lesion and at the level of a bilateral lesion.

Why ?

Course of the SECOND ORDER SENSORY FIBERS ,which originate in the dorsal horn, and ascend for one or two levels as they cross ANTERIOR to CENTRAL CANAL to join the OPPOSITE SPINOTHALAMIC TRACT.

TRANSECTION OF THE CORTICOSPINAL TRACTS,MOTOR TRACTS

Paraplegia or quadriplegia with heightened DTRs ,babinski sign,SPASTICITY.

UPPER MOTOR NEURON SYNDROME –below the level of transection

LOWER MOTOR NEURON SYNDROME – at the level of the lesion.

AUTONOMIC DYSFUNCTION

Absent sweating below the implicated cord level and bowel ,bladder ,sexual dysfunction.

Level of the lesion

Segmental signs corresponding to the disturbed motor and sensory innervation by an individual cord segment.

What could be found at the level of lesion?

A band of altered sensation (hyperalgesia or hyperpathia )

Fasciculations or atrophy in muscles innervated by one or several segments

Muted or absent DTR at the level.

Plus signs of long tract damage

SPINAL CORD DISEASE

SPINAL SHOCK With severe and acute transverse lesions the limbs

may be initially FLACCID rather than SPASTIC.

This state is called as SPINAL SHOCK

May last for several days ,rarely for weeks

D.D – AHC damage over many segments , acute polyneuropathy

The loss of motor function at the time of injury are accompanied by immediate atonic paralysis of bladder and bowel , gastric atony , loss of sensation below a level corresponding to the spinal cord lesion ,muscular flaccidity and almost complete suppression of all spinal segmental reflex activity below the lesion.

SPINAL SHOCK CONTROL OF AUTONOMIC FUNCTION is also

lost below the level of lesion.

Vasomotor tone is abolished –POSTURAL HYPOTENSION

Sweating and piloerection lost – skin becomes dry and pale ,ulcerations develop

Sphincters of bladder and bowel remain CONTRACTED –loss of inhibitory influence of higher centres.

DETRUSOR OF BLADDER AND SMOOTH MUSCLE OF RECTUM ARE ATONIC –OVERFLOW INCONTINENCE

Paralytic ileus

GENITAL RELFEXES ARE ABOLISHED.

BULBOCAVERNOUS REFLEX IS THE FIRST TO RETURN.

CONTRACTION OF THE ANAL SPHINCTER TO BE CHECKED.

F WAVES – ELECTROPHYSIOLOGICAL RESPONSES THAT REFLECT THE FUNCTIONING OF THE MOTOR NEURONS OF THE ISOLATED SEGMENT OF THE CORD APPEAR

WHY DOES SPINAL SHOCK OCCUR?

It is due to the sudden interruption of SUPRASEGMENTAL DESCENDING FIBER SYSTEMS THAT NORMALLY KEEP THE SPINAL MOTOR NEURONS IN A CONTINUOUS STATE OF READINESS.

The facilitatory tracts are the RETICULOSPINAL AND VESTIBULOSPINAL TRACTS.

?CORTICOSPINAL TRACTS.

CERVICAL CORDCERVICAL CORD LEVEL FEATURES

UPPER CERVICAL CORD LEVEL QUADRIPLEGIA,WEAKNESS OF THE DIAPHRAGM

C4-C5 QUADRIPLEGIA

C5-C6 LOSS OF POWER AND REFLEXES IN THE BICEPS

C7 WEAKNESS AFFECTS FINGER AND WRIST EXTENSORS,TRICEPS

C8 FINGER AND WRIST FLEXION

AT ANY LEVEL HORNER’S SYNDROME CAN OCCUR

MIOSIS,FACIAL HYPOHIDROSIS,PTOSIS

Clinical effects

Of Cord lesion

At different

levels

HORNER’S SYNDROME OCULOSYMPATHETIC SYNDROME

BERNARD –HORNER SYNDROME

Interruption of postganglionic sympathetic fibers at any point along the internal carotid arteries or a lesion of the superior cervical ganglion results in miosis,drooping of the eyelid,and abolition of sweating over one side of the face –anhidrosis.

Can also be caused by interupption of the preganglionic fibers.

Interruption of the uncrossed hypothalamospinal pathway in the tegmentum of brainstem or cervical cord.

Tetrad of HORNER’S SYNDROMEm

iosis

ptosis

anhidrosis

*Loss of ciliospinal reflex

CAUSES

1.neoplastic or inflammatory involvement of the cervical lymph nodes or proximal part of brachial plexus.

2.surgical or other types of trauma –jugular venous catheter.

3.carotid artery dissection

4.syringomyelic or traumatic lesions of the first and second thoracic spinal segments

5.infarcts of lateral part of medulla WALLENBERG SYNDROME .

6.idiopathic

If a horner’s syndrome develops early in life ,the iris on the affected side fails to become pigmented and remains blue or mottled gray brown .

HETEROCHROMIA IRIDIS

Horner’s syndrome

STELLATE GANGLION LESION

Compression by a tumor arising from the superior sulcus of the lung (PAN COAST’S TUMOR )

Combination of HORNER’S syndrome plus paralysis of sympathetic reflexes in the limb (the hand and arm are dry and warm)

Preganglionic lesions –facial flushing on the side of sympathetic disorder , increased on exercise (HARLEQUIN EFFECT )

THORACIC CORD

Localisation of the lesion is by the sensory level on the trunk and by the site of midline back pain that may accompany the syndrome.

THORACIC CORD LEVEL

ANATOMICAL SITE

T4 NIPPLES

T7 SCAPULA LOWER BORDER

T10 UMBILICUS

T9-T10 BEEVOR’S SIGN

T12 INGUINAL REGION

dermatomes

LUMBAR CORD

CORD LEVEL FUNCTION LOST

L2-L4 FLEXION AND ADDUCTION OF THE THIGHWEAKEN LEG EXTENSION AT KNEE,LOSS OF KNEE REFLEX

L5-S1 MOVEMENTS OF FOOT AND ANKLE ARE LOSTFLEXION AT KNEE LOSTEXTENSION AT THIGHABOLISH MENT OF ANKLE JERK

CONUS MEDULLARIS Tapered caudal termination of the spinal

cord

It consists of lower sacral and coccygeal segment

It consists of bilateral saddle anesthesia S3-S5

Prominent bladder and bowel dysfunction (urinary retention and incontinence with lax anal tone )

Impotence

Bulbocavernous S2-S4

Anal relfexes S4-S5 are absent.

Muscle strength is preserved

CAUDA EQUINA

IT is the name given to the nerve roots that arise from the cord.

Low back and radicular pain

Asymmetric leg weakness and sensory loss

Variable areflexia in the lower extremities.

Relative sparing of the bowel and bladder function

Cauda equina

A babinski sign indicates that the spinal cord is involved above the fifth lumbar segment

BROWN SEQUARD HEMICORD SYNDROME Ipsilateral weakness (corticospinal tract )

Loss of joint position and vibratory sense (posterior column)

Contralateral loss of pain and temperature sense (spinothalaamic tract ) one or two levels below the level of lesion

Unilateral segmental signs such as radicular pain,muslce atrophy and loss of deep tendon reflex.

Partial forms are more common than fully developed syndrome

Slide of diagram

CENTRAL CORD SYNDROME

Selective damage to the gray matter nerve cells and crossing spinothalamic tracts surrounding the central canal.

Arm weakness out of proportion to leg weakness and a dissosciated sensory loss meaning loss of pain and temperature sensations over the shoulder,lower neck and upper trunk (cape distribution)

Preservation of light touch,joint position,vibration sense in these regions.

Causes –syringomyelia,spinal trauma.

ANTERIOR SPINAL ARTERY SYNDROME

EXTENSIVE BILATERAL destruction that spares the posterior columns.

All spinal cord functions –motor,sensory,autonomic are lost below the level of the lesion,with exception of retained vibration and position sensation.

FORAMEN MAGNUM SYNDROME

Quadriparesis with pain in the back of the head and stiff neck

Weakness and atrophy of the hands and dorsal neck muscles

Marked imbalance

Variable sensory changes

Intracranial extension –signs of cerebellar and lower cranial involvement.

AROUND THE CLOCK progression of weakness –ipsilateral weakness of the shoulder and arm –leg weakness –contralateral leg and finally the contralateral arm.

Suboccipital pain spreading to the neck and shoulders

INTRAMEDULLARYEXTRAMEDULLARY SYNDROMES INTRAMEDULLARY – arise within the substance of

the cord.

EXTRAMEDULLARY –compress the spinal cord or its vascular supply.

Radicular pain is more prominent in extramedullary lesions.

Early sacral sensory loss (lateral spinothalamic tract ) and spastic weakness of legs corticospinal tract due to superficial location of leg fibers in the corticospinal tract

EXTRAMEDULLARY LESIONS

INTRAMEDULLARY LESIONS

RADICULAR PAIN BURNING PAIN

EARLY SENSORY LOSS (SACRAL SENSORY LOSS )

SACRAL SPARING

SPASTIC WEAKNESS IN LEGS (CORTICOSPINAL TRACT )

CORTICOSPINAL FEATURES OCCUR LATER

EXTRADURAL -MALIGNANT

LONG DURATION OF SYMPTOMS

INTRADURAL -BENIGN

COMPRESS THE CORD FROM OUTSIDE

ARISES WITHIN THE SUBSTANCE OF THE CORD

NEOPLASTIC COMPRESSIVE MYELOPATHY

Most are epidural in origin.

High proportion of bone marrow in axial skeleton.

Breast,lung,prostrate,kidney,lymphoma,plasma cell dyscrasias are frequent.

MC to be involved is the thoracic spinal column

Ovarian,prostrate – sacral.lumbar regions – batson’s plexus

Retroperitoneal neoplasms enter through the intervertebral foramens and produce radicular pain with signs of root weakness prior to cord compression

Clinical features

Pain is usually the initial symptom of spinal metastases. aching and localized or sharp and radiating in quality

Typically worsens with movement,coughing,sneezing.awakens the pt at night.

Recent onset of persistent back pain ,particularly if in the thoracic spine should prompt consideration of thoracic metastases.

Plain x rays and radionuclide bone scans may not identify 15-20% of metastatic vertebral lesions and those of origin from intervertebral foramens.

MRI provides excellent anatomic resolution of the extent of spinal tumors.

Distinguishes between malignant and other masses.

MRI

Vertebral metastases are usually HYPOINTENSE relative to a normal bone marrow signal on T1 weighted MRI scans ,after the administration of gadolinium,contrast enhancement may deceptively normalize the appearance of the tumor by increasing the intensity to that of normal bone marrow.

Infections of the spinal column are distinctive in that,unlike tumor ,they may cross the disk space to involve the adjacent vertebral body.

Upto 40 % of patients who present with compression at one level are found to have asymptomatic epidural metastases else where ,thus the length of spine should be imaged when epidural malignancy in question.

Treatment Glucocorticoids –to reduce cord edema Local radiotherapy Specific therapy to the underlying lesion Dexamethasone 40 mg daily Radiotherapy 3000 cGy in 15 daily fractions Good response if ambulatory at presentation. Motor deficits >12 hrs donot usually improve Beyond 48 hrs the prognosis for recovery is poor.

Recurrence usually occurs .. Surgery when the above treatment fails…

INTRADURAL LESIONS

Usually benign

Slow growing

MENINGIOMA

NEUROFIBROMA

Meningioma –located posterior to thoracic cord or near the foramen magnum .

Neurofibromas arise from the posterior root .

Radicular sensory symptoms followed by an asymmetric progressive spinal cord syndrome.

SURGICAL RESECTION

menigioma

NEUROFIBROMA

SPINAL EPIDURAL ABSCESS Clinical triad of midline dorsal

pain ,fever ,progressive limb weakness.

Pain over the spine or radicular pain .

Duration of pain <2 weeks.

Spinal cord damage is because of venous congestion and thrombosis.

MIDLINE DORSAL PAIN

FEVER

PROGRESSIVE LIMB WEAKNESS

Risk are people –diabetes mellitus,renal failure,alcoholism,malignancy,IV drug abuse.

2/3 from hematogenous spread of bacteria from the skin furunculosis,soft tissue pharyngeal abscess,deep viscera.

Predisposing conditions are vertebral osteomyelitis,decubitus ulcers,lumbar puncture,epidural anesthesia,spinal surgery.

Most are due to s.aureus,streptococcus,gram negative

MRI is for diagnosis

Accompanied meningitis <25 % cases.

Organism identified only in presence of meningitis.

Treatment

Decompressive laminectomy

Debridement

Long term anitbiotic treatment

Antibiotics continued for 4 weeks

2/3 patients significantly improve.

ACUTE TRANSVERSE MYELOPATHY

Spinal cord infarction

SLE

Sarcoidosis

Demyelinating disorders –multiple sclerosis,NMO

Post infectious

Infectious

MRI initially to rule out compressive causes

CSF ANALYSIS

OTHER STUDIES BASED ON SUSPICION

SPINAL CORD BLOOD SUPPLY Supplied by three arteries that course vertically

over its surface.

A single anterior spinal artery

Paired posterior spinal arteries

Anterior spinal artery is fed by radicular vessels that arise at C6,at an upper thoracic level,at T11-L2 –artery of Adamkiewicz.

At each segment paired penetrating vessels branch from the anterior spinal artery to supply the anterior two thirds of the spinal cord.

The posterior spinal arteries become less distinct below the mid thoracic level supply the posterior columns.

ischemia

Can occur at any level

Watershed of marginal blood flow in upper thoracic segments by artery of ADAMKIEWICZ

Greatest ischemic risk usually at T3-T4

At boundary zones between anterior and posterior spinal artery territories.

Rapid progressive syndrome over hours of weakness and spasticity with little sensory change.

causes

Aortic atherosclerosis

Dissecting aortic aneurysm

Vertebral artery occlusion

Aortic surgery

profound hypotension from any cause

Treatment---anticoagulation

MULTIPLE SCLEROSIS

May present with acute myelitis in asian or african ancestry.

Mild swelling and edema of the cord and diffuse or multifocal areas of abnormal signal on T 2 weighted images.

Contrast enhancement is present in many cases.

Normal BRAIN scan indicates that the risk of evoltuion to MS is low 10-15% over 5 years.

Multiple periventricular T2bright images –higher risk >50% over 5 years.,90% by 14 years.

Presence of oligoclonal bands –a diagnosis of MS is more likely.

Treatment

IV METHYLPREDNISOLONE 500 mg over 3 days

Oral prednisolone 1 mg/kg /day for several weeks then taper

Plasma exchange …

POSTINFECTIOUS MYELITIS

Follow an infection or vaccination

EBV,CMV,mycoplasma,influenza,measles,varicella,rubella

Begins as the patient appears to be recovering from an an acute febrile infection

No organism could be isolated from nervous system or spinal fluid.

It represents an autoimmune disorder triggered by infection ..

Treatment –glucocorticoids ,plasma exchange

SPONDYLITIC MYELOPATHY Most common cause of chronic cord

compression

Neck and shoulder pain with stiffness are early symptoms

Radicular arm pain in a C5 or C 6 distribution.

Compression of cervical cord <1/3 cases

Slowly progressive spastic paraparesis

Asymmetric

Paresthesias in feets and hands

Diminished vibration sense in legs

Postive romberg’s sign

Diminshed DTR mostly at the level of biceps

Dermatomal sensory loss in arms atrophy of intrinsic hand muscles increased DTR in legs extensor plantar responses

Treatment

Plain x rays are less useful’

MRI

T2 WEIGHTED images –reveal areas of high signal intensity within the cord adjacent to the site of compression.

Cervical collar

Surgical decompression

Posterior laminectomy

Anterior apporach with disk resection

SYRINGOMYELIA Developmental cavity of the cervical cord that is

prone to enlarge and produce progressive myelopathy.

Begin insidiously in adolescence or early adulthood,progress irregularly ,and may undergo spontaneuos arrest for several years.

Cervical thoracic scoliosis

>50% chiari type I malformation –cerebellar tonsils protrude through the foramen magnum and into the cervical spinal canal.

Interference with CSF flow is likely for expansion.

Acquired cavitations of the cord in areas of necrosis are also termed syrinx cavities –follow trauma,myleitis,chronic arachnoiditis

Presentation is of central cord syndrome

Most cases begin asymmetrically with u/l sensory loss over hands

Muscle wasting in the lower neck ,shoulders,arms and hands with asymmetric or absent reflexes in arms –expansion of the cavity into the gray matter of the cord.

Further enlargement of the cavity – spasticity and weakness of the legs,bladder and bowel dysfunction,horner’s syndrome

Facial numbness –c2

Cough induced headache and neck arm pain

Palatal or vocal cord paralysis –syringobulbia

MRI of brain and whole spinal cord needed

Treatment

Suboccipital craniectomy –chiari tonsillar herniation

Upper cervical laminectomy

Placement of dural graft

SUBACUTE COMBINED DEGENERATION Paresthesias in hands and feet

Loss of vibration and position sensation

Progressive spastic and ataxic weakness.

Loss of reflexes due to peripheral neuropathy plus a positive babinski sign is an imp diagnostic clue.

optic atrophy and irritability may be prominent in advanced cases but are rarely the presenting symptoms

Diffuse rather than focal

Signs are generally symmetric

Predominant involvement of posterior and lateral tracts

Positive romberg’s sign.

Diagnosis by finding of macrocytic RBC,low serum b12 conc,elevated levels of serum homocysteine,methylmalonic acid.

Treatment – 1000ug of IM vitamin b12

Posterior columns

Are Affected

in SACD

COGNITIVE DYSFUNCTION AS

A RESULT OF VIT B12 DEFICIENCY

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