Quadriparesis of human beings due to compression.pptx

Weakness of all 4 limbs

1. - INTRODUCTION Progressive spastic paraparesis/ quadriparesis is most commonly due to spinal cord pathology, which is suggested by Bilateral upper motor neuron signs, Sensory deficits, Bladder/bowel/sexual dysfunction.

2. HISTORY Age: young vs old Onset and Duration : Is it acute­ within minutes or hours? Is it subacute­ within days or weeks? Is it chronic­ within months or years? Progression of weakness: constant/progressing/intermittent

3. History of : Trauma to cervical spine Pain in neck History regarding infections/fever(Viral illness/Tuberculosis ) Any comorbid illness: Diabetes, Hypothyroidism, HIV Any loss of sensation Bowel and bladder involved or not?

4. QUADRIPARESIS " , UMN SIGNS LMN SIGNS , ' . • , BRAIN SPINAL CORD (Cervical) Compressive Non Compressive - Anterior horn cell - Roots - Nerves - Neuro-muscular jn - Muscle

5. Approach to UMN Lesions Cerebral Palsy- leading to spastic quadriplegia along with other associated features Young adult/quadriparesis along with visual disturbances(one or more episodes)/relapses and remissions – Multiple sclerosis Consciousness retained/paralysis of limbs and oral structures/ voluntary blinking and vertical eye movements remain intact

6. SPINAL CORD LESIONS Lesions may be Extradural – It can be cervical compressive myelopathy, Tuberculosis( pott’s spine), neoplastic conditions (most commonly – metastasis, multiple myeloma) , extradural haematoises (anaemia, thalassemia) ands other rare infections like syphilis, blastomycosis Intradural extra medullary – They may be spinal meningioma, neuroenteric cyst, spinal AV malformations Intra medullary – Ependymoma , astrocytoma, hemangioma , multiple sclerosis, sarcidosis

7. A pp roach to UMN Lesions :cervical Cord FEATURE S COMPRESSIVE NON- COMPRESSIVE Bony deformity Bony tenderness Upper level of sensory loss Root pain Onset and progress Symmetry Bladder and bowel involvement Present Present present Present Gradual Asymmetrical Late Absent Absent Absent Absent May be acute Majority are symmetrical Early(acute transverse myelitis)

8. Features ExtrameduIlary IntrameduIlary Radicular pain Funicular pain Motor deficit Common Rare Ascending motor weakness .i.e. Sacral>lumbar> thoracic> cervical Unusual Common Descending pattern of loss .i.e. Cervical >thoracic>lumbar> sacral Reflexes Sensory deficit Brisk, early feature Ascending sensory loss.Le. Sacral>lumbar> thoracic> cervical less brisk. Descending pattern of loss .i.e. Cervical >thoracic>lumbar> sacral Dissociative sensory loss Sacral sensastions Bowels and bladder involvement Lost early Late Sacral sparing Early

9. Lesion at Foramen Magnum: Motor: ''Around the clock'' type of motor weakness may be seen (Ellsberg phenomenon) Sensory: Suboccipital pain in the distribution of great occipital nerve Downbeat nystagmus Cerebellar Ataxia Papilledema ( Due to CSF obstruction} sp i nal cord C1 Occipetal bone F magnum C2

10. Lesions of High Cervical Cord Cl- C4 Pain at suboccipital region(C2 ) Lhermitte's symptoms: Due to lesions of posterior cord Electric shock like sensations radiating down spine which may be transmitted to extremities & may occur with neck flexion Inability to elevate shoulders(Compromise of Cr. N XI supplying Sternocleidomastoid and Trapezius in compressive lesions of C1- C4)

11. Lesions of high Cervical Cord Cl- C4 Diaphragmatic paralysis(particularly lesions involving C3- C 5 ) False localizing signs including thoracic sensory levels, proprioceptive sensory loss, paraesthesias of hands, clumsiness and atrophy of hands can occur with disorders afflicting upper cervical cord Biceps jerk(C5,C6) Exaggerated

12. Lesions of H ig h Cervical Cord CAUSES: Cervical spondylosis Tumors(Meningioma, neurofibroma, gliomas) Basilar invagination(e.g in Pagets Disease) Cranio- vertebral junction anomalies Atlanta-axial subluxation( e.g. Rheumatoid Arthritis) Multiple Sclerosis Syringomyelia Chiari- 1 Malformation Morquio disease

13. Lesions affecting C5-C6 Lesions affecting C 5 &C6 leads to LMN paresis of arms and spastic paresis of lower extremities. Diaphragmatic functions may be compromised ( C5 affection) ► Lesions at C 5 : Sensory loss over entire body below neck. Biceps jerk(C 5 ,C6 ) Brachioradialis jerk(C 5 -C6 ) _ Triceps reflex(C6- C7) Finger flexion reflex(C8- T1) Absent/Diminished Exaggerated

14. ► Lesions at C6: Upper Extremity Oermatome Anterior V iew Lineage Sensory loss over entire body below neck except that lateral arm is spared Biceps jerk(C 5 ,C6 ) Brachioradialis jerk(C 5 - C6 ) Triceps reflex(C6- C7) Finger flexion reflex(C8- Tl) } Depressed/ Absent Exaggerated

15. ► Lesions at C7: Sensory loss at and below the third and 3 rd and 4 th digits(including the medial arm and forearm) Paresis involves the flexors and extensors of wrists and fingers Biceps jerk(C 5 ,C6 ) Brachioradialis jerk(C 5 - C6 ) Finger flexion reflex(C8- Tl) Preserved Paradoxical triceps reflex may be seen(flexion of elbow in percussion to triceps tendon)- afferent arch of triceps reflex is injured in injuries of C7

16. Lesions affecting C8-T1 Sensory loss involves the fifth digit and the medial forearm and arm as well as the rest of the body below the lesion. Weakness predominantly involves the small hand muscles with associated spastic paraparesis Biceps jerk(C 5 ,C6 ) Brachioradialis jerk(C 5 - C6 ) Triceps reflex(C6- C7) Finger flexion reflex(C8- T1) Preserved Diminished May be associated with unilateral or bilateral Horner Syndrome

17. Syringomyelia Fluid filled, gliosis lined cavity within spinal cord(mostly b/w C2- T9) Symptoms more pronounced in upper limbs- Distal muscle wasting seen ''Suspended'' and ''dissociated'' sensory loss- loss of pain & temperature sense with preserved light touch, joint position and vibration sense or.so t pn,n Qnd t erni;:> rcs t u l"e s on :ae • llon l- .A h JJtr" I ec:>r-1- ICO•s>•n &.a1t tr.R C: I o f' UPP- 01" motor nourona f'\auron• S yrin go my e l i a of the Ce rv i ca l Co rd

18. Motor Neuron Disease Degenerative disease of the motor neurons in which both UMNs and LMN are involved almost exclusively. Course is not relapsing and remitting, but rather INSIDIOUSLY PROGRESSIVE UMN+LMN- myotrophic Lateral Sclerosis(ALS )- MOST COMMON Can be associated with bulbar/pseudobulbar palsy. Asymmetric limb weakness is the most common presentation. Upper extremity onset is most often heralded by hand weakness and lower extremity onset of A LS most often begins with foot drop Cognitive functions are usually preserved

19. The dia g nosis of A LS is further suggested by an Absence of histor y of : Neuropathic or radiculopathic pain Sensory loss Bladder and bowel involvement Ptosis ( Motor neurons for ocular motility remain unaffected)

20. Sub acute combined degeneration of Spinal cord Vit . B12 deficiency leading to degeneration of dorsal and lateral white matter of spinal cord DORSAL COLUMN Impaired tactile discrimi nation, proprioception, vibration sense LATERAL CORTICOSPINAL TRACT Muscle weakness Hyperreflexia Spasticity Paraplegia/quadriplegia Bladder and bowel involvement in advanced cases SPINOCEREBELLAR TRACT Sensory Ataxia (Romberg sign)

21. Anterior spinal artery syndrome Abrupt onset of symptoms Loss of motor functions, pain/temperature sensations Relative sparing of proprioception and vibratory sense below the level of lesion S L T C . .. --- - I , :• .. . .- , . . . .. . . . . . . . . . . • . . - . ·,:·.·.- :. : '• I • , • . I . • • • •. " .. . . . • \ I . :_·. - ' · . . ::_._ : - :·: ': .':':: . '{:. :·· . _,: , : - :· · . ' '- " " / :·:,:. f,,,,.:.:, ... .., ·. ,. ....- ....- ....... ... . .... . -- - Anterior Co 1 rd Syndrome \Vat crshed region of blood supply to th e cerv i ca l cord. ' l 'rnc t lan1ination: C = cervica l ;' I' = th oracic; L = lwnbar ;S = sacra l.

22. INVESTIGATIONS Commonest investigation used in this patient is CEMRI MRI of the spinal cord will help confirm the lesion location and pattern, which helps to narrow the differential diagnosis . The entire spinal cord should be imaged to avoid false negative results that may be caused by misleading localizing sign, such as a thoracic sensory level caused by a cervical lesion. It is essential that MRI be of high quality with ≥1.5 T (T) magnet, and include T1-weighted (T1WI) sequences with and without Gadolinium ( Gd ), as well as T2-weighted ( T2WI)gradient echo(GRE), fast spin echo(FSE ), and shortT1inversion recovery (STIR) sequences.

23. Diagnosis of spondylitic myelopathy is usually straightforward when MRI of the spinal cord demonstrates overt cord compression Spondylitic changes may be associated with extensive T2 hyperintense intramedullary signal and transverse band of Gd enhancement at the region of maximal spinal cord compression

24. Degenerative disk disease can also cause dynamic cord compression that may require flexion–extension X-ray or MRI. Flexion position MRI may reveal another 12% of cases with narrowing of subarachnoid space that is not visible in the neutral position.

25. Conventional MRI may also be inadequate for evaluating ligamentous calcifications in degenerative spine disease and other conditions of increased calcium deposits, such as ectopic tumoral calcinosis, a complication of systemic sclerosis/scleroderma. Computerized tomography(CT)is the preferred imaging modality when calcification is suspected