CLINICAL EXAMINATION OF A CASE OF PARAPLEGIA

                                                            . PARAPLEGIA

Clinical Examination of a case of Paraplegia

HISTORY: PRESENT HISTORY:

Symptoms to be elicited

1. Motor symptoms

2. Sensory symptoms

Plus Symptoms of

3. Sphincter disturbances,

4. Lesions of Higher functions,

5. Cranial Nerve lesions.

 Motor symptoms

Enquire if

« Paralysis or paresis.

   If limb involvement was ¨symmetrical or serial

¨Distal or proximal involvement

  Distal- presents as foot drop or frequent tripping

   Proximal as –difficulty in getting up from sitting posture,

   Difficulty in walking, running or climbing stairs.

 ¨Ask about wobbling while standing –suggestive of hypotonia.

   Ask about symptom of stiffness or crossing of limbs while walking 

   suggestive of hypertonia.

  ¨Elicit history of involuntary movements.

 Sensory symptoms

 Elicit the history of following.

 «Anesthesia or hypoesthesia of the limbs

 «Parasthesia

 «Root pain –aggravates on coughing or straining.

 Sphincter disturbances

ªUrgency, precipitancy or hesitancy.

ªRetention with overflow.

ªIncontinence (true or false)

ªPainless bladder distension.

ªPainful bladder distension.

 Symptoms pertaining to higher functions

 Alterations in sensorium- occur in cortical paraplegia.

 Euphoria can occur in multiple sclerosis /long term cortisone therapy.

 Mental deterioration in- Pagets with skull involvement.

 Cranial Nerve dysfunction in paraplegia:

I cranial nerve may be involved in Taboperisis.

II.cranial nerve in

 Multiple sclerosis.

Tabes (optic atrophy)

Spinocerebellar degeneration (retinitis pigmentosa)

SMON –Sub acute myelo optic neuropathy

Pappiloedema/optic neuritis in Gullian Barre syndrome.

III, IV, VI

 External ophtholmoplegia can occur in Gullian Barre.

V cranial nerve (descending tract of Trigeminal)

 in high cervical cord lesion.

VI cranial nerve

 – in cortical paraplegia like tumor of Falx Cerebri. (False localizing sign)

VII cranial nerve LMN type

 –in Gullian Barre.

VIII cranial Nerve

–in Madras Motor neurone Disease

  (Sensory neuronal deafness)

IX, X, XII

in –MND –bulbar or pseudo bulbar type.

Pharyngeal palsy with dysphagia in Gullian Barre

Cranial polyneuritis in Gullian Barre

CVJunction anomaly.

Multiple cranial Nerve involvement in Paget’s

(1^st, 2nd, 6th, 8th and lower cranial nerves)

  

 History

 Other points to be elicited in present history

Onset and progress.

Onset

Paraplegia of acute onset

1.   Trauma of vertebral column.

2.   Intervertebral Disc Prolapse

3.   Acute transverse myelitis.

4.   Anterior spinal artery thrombosis.

5.   Hematomyelia.

6.   Gullian Barre.

7.   Bleed into a spinal cord tumor.

Sub acute onset

 Spinal epidural Abscess.

Insidious Onset

Compressive and non-compressive myelopathy.

PAST HISTORY

Trauma

 Direct trauma,

 IVdisc prolapse due to lifting of heavy weights

Inflammatory

Infections

 TB, syphilis,viral,(Rabies, HIV),Rickettsial,Fungal like Actinomycosis,Cryptococcus

Neoplastic

 H/O tumors in the past, which can cause secondaries in the spine.

Metabolic

 h/o Liver disease, porphyria.

Immuno-Allergic

 H/o Vaccination-Rabies, tetanus, Polio

H/exanthemata,-Chicken pox, measles

Physical

 H/O irradiation, Electric Shock

Toxins

 Kesari Dal Intake, lathyrism, triorthocresyl phosphate

Occupational History

Divers, Miners -(Caissons Disease).

PERSONAL HISTORY

DM, HT, IHD, Atherosclerosis (Anterior Spinal Artery thrombosis).

Alcoholism: Myopathy.

H/o Living in Endemic area: of or flurosis.

GENERAL EXAMINATION:

Neurofibromata,

Cafeau-laits spots,

Subcutaneous nodules (secondaries)

Spider nevi

Kyphosis, scoliosis, Pescavus (spino cerebellar degeneration)

Icthyosis-SACD, Pellagra

Trophic ulcer- Syrinx, Tabes

Fasciculation.

EXAMINATION OF SPINAL MOTOR SYSTEM

Examine to find if given case is one of UMN lesion or LMN lesion.

EXAMINATION OF SENSORY SYSTEM

Determine if there is sensory loss and

if so, if there is a definite horizontal level for the sensory loss.

If present, possibilities are:

Transverse myelitis-if of acute onset

Cord compression –if of insidious onset

Occasionally rapidly growing spinal tumor may present like acute flaccid paraplegia.

EXAMINATION OF SPINE (VERTEBERAL COLUMN)

Gibbus

Kyphosis, scoliosis

Tenderness

Para vertebral swelling (infection or malignant disease)

Tuft of hair/sacral dimple –Spina bifida occulta/Dermoid.

Straight Leg Raising Test: if positive –indicates root lesion.

Restricted spinal mobility –indicates bone disorder/disc disease/root disease.

                            

Most common causes of Paraplegia Trauma Tumor Tuberculosis Thrombosis Transverse myelitis

                                                     Figure 1and 2. CAUSES OF PARAPLEGIA 

COMPRESSIVE MYELOPATHY.

Pathogenesis of cord involvement:

1. Direct involvement of roots and cords causing dysfunction.  

2. Can interefere with longitudinal and radicular spinal arteries causing ischemia of the segment, which they supply.

This vascular disturbance causes local edema of the cord. This  results in degeneration of the white matter- areas of softening occur.( called compressive myelitis.)

3. Compression can cause pressure effect upon ascending longitudinal spinal vein, which leads to edema of the cord below the site of compression

e.g. If there is compression at high cervical level edema can occur at C8T1 level resulting in small muscle wasting.

Order of compression of the tract:

1st Pyramidal tract,

then Posterior column,

lastly Spinothalamic tract.

But exception can occur to this rule.

Explanation for the above;

vPyramidal tract is supplied by the terminal branches of spinal arteries and hence most susceptible to compressive ischemia.

vAnother explanation offered:

Pyramidal tract is lying closest to denticulate ligament

This ligament is subject to traction in spinal cord compression.

So pyramidal, tract is most involved.

Obstruction of subarachnoid space,

below the level of the tumor. causes loculation of CSF

-causing the characteristic changes in its composition.

                               CAUSES OF COMPRESSIVE MYELOPATHY

  

 Elsburg phenomenon; Order of involvement of limbs: 1st Upper limb of one side next L.limb of same side, going on to lower limb of opposite side,finally Upperlimb of that side.(U’Shaped involvement)Occurs in compressive cervical myelopathy-but not in all cases.

Differences between Extradural and Intradural lesions.

Extra dural	Intra dural
Pain-present -(root pain and spinal tenderness)	Anesthesia present –Dissociated anesthesia.
Pyramidal involvement –early.	Bladder involvement early.
Proteins in CSF-High.	Not so high.
Asymmetrical	Symmetrical involvement
	Trophic Ulcers common

Points, which help in determining level of lesion in spinal cord -compression:

1. Sensory level

2. Motor level

3. Reflex level

4. Root pain-shows dermatome involved.

5.  Type of bladder involvement.

6. Autonomic disturbances.

Sensory level:

Below that level, sensory loss or impairement.

Motor level:

1.Beevor’s sign:- T10 lesion; Umbilicus moves up on raising the head,

because lower abdominal muscles are weak. The upper abdominal muscles supplied by T8-T10 pull the umbilicus up.

Reflex level:

Inverted supinator reflex indicates level of lesion is C5.

If upper abdominal reflexes are preserved & lower abdominal are preserved the level of the lesion is T10.

Autonomic disturbances:

Below a certain level there will be autonomic disturbances like loss of sweating or excessive sweating, loss of temperature or pilo erection.

                     NON-COMPRESSIVE MYELOPATHY.

Infective Causes: Bacterial: Acute: Staphylococcal (extramural or intradural) Chronic: Tuberculous, Syphilitic.

Parasitic: Hydatid, cysticercosis, Schistosomiasis, falciparum malaria.

Viral: Polio, Rabies, Herpes zoster,HIV

Rickettsial: Typhus fever, spotted fever

Fungal: Cryptococcus, Actinomycosis, and coccidiomycosis

Immuno Allergic causes:

Post vaccinial-Rabies, tetanus, and polio

Post exanthematous-Chicken pox, Herpes zoster

Demyelinating:

Multiple sclerosis, Neuromyelitis optica,

Sub acute combined degeneration.

Transverse Myelitis can be due to infective or immuno allergic or Demyelinating causes.

 

 Heredo familial, Degenerative:

Spinocerebellar degeneration.

Familial spastic paraplegia

Motor neuron Disease

Toxic myelopathy:

Lathyrism

TOCP

Arsenic

Contrast media used in radiology

Intra thecal penicillin

Spinal anesthesia

SMON-Sub acute myelo opotic neuropathy (long term enteroquinol, large dose; Myelopotic and peripheral neuropathy. Abdominal symptoms.

Vascular Disorder:

Arteriosclerosis-Anterior spinal artery thrombosis

Dissecting aneurysm of aorta

AV malformation

2ndry to surgery on aorta

Metabolic /Nutrional;

B12 deficiency. Pellagra, Myelopathy of chronic liver disease

Tropical;

Tropical spastic paraplegia

Para Neoplastic Syndrome:

Physical agents;

Irradiation

Electric shock to spinal cord

Caisson’s disease.

Manifestations of cord /root lesion depends upon

1. Level of lesion

2. Speed of onset

3. Vascular involvement 4. Site

Level of the lesion:

AboveL1 vertebra- Damage to both cord and roots.

Below L1 vertebra- only roots are involved.

Speed of the lesion:

A rapidly progressive cord lesion produces flaccid paralysis and absent reflexes and extensor plantar. This is similar to spinal shock in trauma.

After weeks or days tone becomes hypertonic.

Vascular involvement:

In cord compression damage may be due to mechanical stretching or ischemia.In certain cases clinical findings indicatecord damage well beyond the site of compression. This shows vessel compression at the site of lesion is causing distant ischemic effect.

Site of lesion:

Intra medullary lesion produces only segmental signs &symptoms.

Extra dural lesions on the other hand produce both signs of root lesion cord lesion.

i.e. At the site of lesion –LMN segmental lesion with segmental sensory loss & below that level-UMN Lesion & sensory loss plus root pain.

DIAGNOSIS OF LEVEL OF THE LESION.

Upper cervical region& foramen magnum:

1. Severe pain in the occiput &neck.
2. In hands loss of loss of posterior column sensation is early symptom &severe tingling &numbness.

Pain & weakness in the limbs & wasting may occur in the upper limb.

3. Movements of diaphragm reduced because of compression of phrenic nerve.
4. Lower cranial nerve involvement &medullary involvement can occur.
5. Descending tract of trigeminal can be involved.

C5C6 segment lesion:

1.   Inverted supinator reflex

2.   wasting of muscles supplied byC5C6 namely deltoid,biceps,

3.   brachioradialis,infra & suprasinators&rhomboids

4.   Paraplegia

C8T1 Level:

 1. Wasting of small muscles of the hand.

 2. Wasting of flexors of wrist & fingers.

 3.  Horner’s syndrome.

 4.  DTR of upper limbs preserved.

 5.  Spastic paralysis of trunk & lower limbs.

Cervical spondylosis never involves C8& so small muscle wasting rules out cervical spondylosis.

Mid Thoracic region of spinal cord:

1.   Upper limb normal.

2.   Wasting of intercostals muscles (those supplied by involved segments)

3.   .Movements of diaphragm normal.

4.   Spastic paralysis of abdominal muscles &lower limbs.

9th &10^th thoracic segments:

1. Beevor’s sign

(when patient raises the head against resistance umbilicus is drawn upwards).

T12L1 segments:

Abdominal reflexes preserved

Cremastric lost.

Paraplegia

Wasting of internal oblique & transverse abdominal muscle.

L3 L4 segmental lesion:

1. Flexion of hip is preserved.

2. Cremastric preserved.

3. But Quadriceps & adductors of hip are wasted

4. Knee jerk is lost or diminished.

5. But ankle jerk is exaggerated.

6. Plantar-extensor.

7. Foot drop plus.

S1S2 segments; 

1.   Wasting & paralysis of intrinsic muscles of feet.

2.   Wasting & paralysis of calf muscles Plantor flexion impaired.

3.    But dorsi flexion of foot is preserved.

4.    In the hip all muscles of hip are preserved except flexors & adductors.

5.   In the knee flexors of knee are wasted.

6.   Knee jerk is preserved

7.   Ankle jerk is lost.

8.   Plantar reflex is lost.

9.   No foot drop.

10. Anal & Bulbocavernous reflexes are preserved.

S3S4 segments:

1 .Large bowel & bladder are paralysed.

2. There is retension of urine & feaces due to unopposed action of internal sphincters.

1. The external sphincters are paralyzed.

2. Anal & bulbo cavernous reflexes are lost.

3. Saddle shaped anesthesia occurs.

4. but no paraplegia.

 Difference between Cauda equine & Conus lesion

Differenciation is often difficult.

Cauda equina lesion :produces

Asymmetric,

Atonic,

Areflexic,

Paraperisis;

With bladder & bowel disturbance

Plus sensory loss

Saddle shaped anesthesia

Pain is common & is referred to perineum & thigh.

Conus lesion

¬In spite of paralysis of bladder &rectum if bulbocavernous and  anal reflexes are preserved and

¬If there is dissociated sensory loss (over ?S2S3S4),

it is likely that the lesion is  in conus.

¬If the lesion extends above S1 then plantar can be extensor,which is never the case with cauda lesion.

Features	Cauda lesions	Conus lesions(S3,S4,S5,C1)
Pain	Pain in lower limbs is characteristic.	Often absent or limited to buttocks &perineum.
Bladder and  rectal symptoms.	Often absent Present only in the involvement of lower sacral roots-usually late.	Always present
Symmetry	Often asymmetrical or unilateral for along time.	Practically always bilateral.
Sensation	All forms of sensation impaired.	May be dissociated.
DTR	Both knee & ankle jerk Lost.	Only ankle jerk affected/or even that may be spared.
Tone	Flaccid paralysis of legs &feet characteristic of cauda lesion.
Trophic changes	Absent	Present.

Investigations in a case of paraplegia

Plain Xray Spine

Myelogram

CT scan

CSF analysis

Plain Xray Spine

Lateral and oblique view:

Signs of degeneration of spines

 Reduction of intervertebral space

 Narrowing of intervertebral foramina

 Osteophyte  formation.

Widening of IV foramina-Neuro fibroma

Widening of inter peduncular distance:-long standing intramedullary, intradural lesion.

Secondaries,myeloma,tuberculous infection:

Destruction of vertebra/collapse of vertebra..

AP view:

Erosion of the pedicle-extra medullary tumor

Para spinal mass; -extra medullary tumor /cold abscess.

Myelogram (Must specify at which level lesion is suspected.)

A. Extradural:

  Complete block shows with 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.

  Partial block;

Extra dural; Dura mator is lifted away from the vertebral body.

B. Intra dural;

  Intra medullary; contrast is splayed arounddilated cord.

  Extramedullary; cor displaced to one side.

CSF Analysis;Lumbar puncture can worsen neurological disease, because of the pressure gradient itcreates.So when a compressive lesion is suspected lumbar puncture &CSF analysis can be done at the time of Myelography.

CSF protein is increased often especially below the block,more so in extra medullary.

Cell count; Increase in Leukocytoes indicates infections like Abcess/TB.

Queckenstedt’s Test:

Absence of pressure transmission to the CSF during lumbar puncture ’when the neck veins are compressed.

Positive test indicates complete block.

CT scan:

Plain CT; Can diagnose narrowing of disc disease of lu8mbar region.

Can identify narrowing of lumbar canal& thickening of facet joint.

Contrast CT is required to show Cord compression.:

Best done 6-12 hrs after myelography.

Can show amount of compression & delineate neurofibroma likeintraspinal lesions..

MRI:

Saggital views are to be taken., not axial views as in case of CT scan.

Can differentiate Syringomyelia from intramedullary tumors.

Other investigations;

➼Xray chest: May show P.T,Lymphomaor malignancy.

➼C.S.F.-Electrophoresis to show oligoclonal bands of multiple sclerosis.

➼Serological tests for Syphilis.

➼IgG/Albumin ratio-to diagnose multiple sclerosis.

PPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPPP