Approach to quadriparesis

QUADRIPARESIS- Clinical approach

1. Approach To A Case Of Quadriparesis - Dr DEEPAK SHARMA JR3 Dr. DAVID JR3

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

3. History of : Trauma to cervical spine Pain in neck Recent history of vaccination(Rabies, H1N1, COVID) History regarding infections/fever(Viral illness/Tuberculosis) Any comorbid illness: Diabetes, Hypothyroidism, HIV

4. History of: Any loss of sensations? Any sphincter disturbances( bladder and bowel involvement) ?

5. Past History : Enquire about Malignancy; Swellings or bone tenderness? Surgery for tumors? Chemotherapy or radiation? Personal History : diet(veg/non veg, vitamins deficiencies, excess alcohol intake), Drugs intake Occupational exposure (regarding toxins(OP), heavy metals) Family history: hereditary? Familial periodic paralysis ALWAYS RULE OUT MALINGERING IF HISTORY IS NOT SUGGESTIVE OF ANY NEUROLOGICAL DISEASE.

6. - Anterior horn cell - Roots - Nerves - Neuro-muscular jn - Muscle QUADRIPARESIS UMN SIGNS LMN SIGNS BRAIN SPINAL CORD (Cervical) Compressive Non Compressive

7. 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

8. Approach to UMN Lesions Consciousness retained/paralysis of limbs and oral structures/ voluntary blinking and vertical eye movements remain intact Bilateral ventral pontine damage LOCKED IN SYNDROME

9. Approach to UMN Lesions(Cervical Cord) FEATURES COMPRESSIVE NON-COMPRESSIVE Bony deformity Present Absent Bony tenderness Present Absent Upper level of sensory loss present Absent Root pain Present Absent Onset and progress Gradual May be acute Symmetry Asymmetrical Majority are symmetrical Bladder and bowel involvement Late Early(acute transverse myelitis)

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

11. 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 )

12. Lesions of High Cervical Cord(C1-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)

13. Lesions of High Cervical Cord(C1-C4) Diaphragmatic paralysis(particularly lesions involving C3-C5) Biceps jerk(C5,C6) Exhaggerated 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.(? Ant. Spinal artery ischemia, venous congestion ) { Sonstein et al, 1996}- {Localization in Clinical Neurology, 6 th edition}

14. Lesions of High Cervical Cord(C1-C4) CAUSES: Cervical spondylosis Tumors(Meningioma, neurofibroma, gliomas) Basilar invagination( e.g in Pagets Disease) Cranio-vertebral junction anomalies Atlanto -axial subluxation( e.g. Rheumatoid Arthritis) Multiple Sclerosis Syringomyelia Chiari-I Malformation Morquio disease

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

16. Lesions at C6: Sensory loss over entire body below neck except that lateral arm is spared Biceps jerk(C5,C6) Brachioradialis jerk(C5-C6) Triceps reflex(C6-C7) Finger flexion reflex(C8-T1) Depressed/Absent Exaggerated

17. 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(C5,C6) Brachioradialis jerk(C5-C6) Finger flexion reflex(C8-T1) 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 Preserved Exaggerated

18. 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(C5,C6) Brachioradialis jerk(C5-C6) Triceps reflex(C6-C7) Finger flexion reflex(C8-T1) May be associated with unilateral or bilateral Horner Syndrome Preserved Diminished

19. 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

20. 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- Amyotrophic 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 ALS most often begins with foot drop Cognitive functions are usually preserved

21. The diagnosis of ALS is further suggested by an ABSENCE of history of : Neuropathic or radiculopathic pain Sensory loss Bladder and bowel involvement Ptosis (Motor neurons for ocular motility remain unaffected)

22. 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 discrimination, 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)

23. 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

24. QUADRIPARESIS Sensory level on examination yes Compressive myelopathy Non compressive myelopathy, Transverse myelitis Deep Tendon Reflexes No Symmetric ascending paralysis GBS Ocular/bulbar involvement + Fluctuating weakness, fatigue Myasthenia Gravis Descending weakness , bradycardia Botulism Neurotoxic snake bite Intermittent weakness, precipitating factors Periodic paralysis Symmetric proximal muscle weakness Dematomyositis , polymyositis Prolonged ICU stay, sepsis Critical illness polyneuropathy