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Approach to a case of paraparesis .pptx
- 1. Approach to Paraparesis Moderator:Dr.Diganta Das Assistant Professor Dept. of General Medicine Presenter :Dr. Shyamjith Lakshmanan B 1st Year PGT Dept. of General Medicine
- 2. Definition •Impairment in motorfunction of lower extremities with or without involvement of sensory system •Weakness of Bilateral lower limbs is called Paraparesis. •Complete paralysis of Bilateral lower limbs is called paraplegia.
- 3. Approach to apatient with Paraparesis • HISTORY : – Mode of onset : Sudden or Gradual – Duration Of Symptoms : Short or Long – Progression of paralysis : Symmetrical or Serial Proximal or Distal muscle Weakness is progressive or static – Sensory Involvement – Bladder and Bowel Involvement
- 4. – Associated symptoms: Fever,Seizure, etc. – Past h/o tuberculosis, fever, diarrhoea, primary chancre – History of Trauma,Prior vaccination – Dietary history – Occupational history
- 5. Examination Complete System Examinationwith Detailed Nervous System Examination To be done CNS Examination •Higher Mental Function •Cranial Nerve Examination •Motor System : Tone Deep Tendon Reflex • Sensory System
- 6. Localization of theLevel of Lesion • Principle 1 : • To determine the motor, sensory and reflex level independent of each other • Highest of the three levels is chosen • Principle 2 : • Below the level of lesion : UMN weakness + spasticity + Exaggerated reflexes + complete sensory loss • At the level of lesion : LMN weakness + Loss of reflexes + Root pain • Upper border of sensory loss : Examination of the patient from below upwards • Girdle like sensation or sense of constriction at the level of lesion
- 7. • Zone ofhyperaesthesia or hyperalgesia • Analysis of the abdominal reflex • Analysis of the deep reflexes • Examination of vertebrae
- 8. Features of Spinalcord Lesion at Specific Level • Cervical cord lesion : • C5 – C6 level : weakness of biceps • C7 : Finger and wrist extensors and triceps • C8 : Finger and wrist flexion • Thoracic cord lesion : • Localization is done by sensory level (Important markers are nipples T4 and Umbillicus T10) • Weakness of lower limbs • Bladder and bowel involvement • Beevor’s Sign
- 9. • Lumbar cordinvolvement : – L2 – L4 : Loss of flexion and adduction of thigh Loss of Leg extension at thigh Loss of patellar reflex – L5 – S1 : Movements of foot and ankle Flexion at knee Extension at the thigh Ankle jerk
- 11. Paraplegia : LMNand UMN types Upper Motor Neuron Lesion (Spastic) Intracranial Spinal cord Lower Motor Neuron Lesion (Flaccid) Anterior horn cells Roots Peripheral nerves Myo-Neuronal Junction Muscles
- 12. Spastic Paraplegia FlaccidParaplegia Muscle atrophy Absent or Late Early and Prominent Muscle Tone Hypertonia Hypotonia Motor power Loss Partial Complete Deep tendon Reflex Increased Absent Clonus Present Absent Plantar Reflex Extensor Flexor or Absent
- 13. Cerebral causes Gradual Onset •Cerebraldiplegia •parasagittal meningioma •hydrocephalus SUDDEN ONSET: • Thrombosis of unpaired anterior cerebral artery • superior sagittal sinus thrombosis • Injury at paracentral lobule
- 14. Clinical Features ofCerebral Causes of Paraparesis •Spastic Paraplegia •Lack of sensory Symptom •Early bladder symptoms •Headache •Vomiting •Seizure
- 15. Spinal Cord Disorders 1.COMPRESSIVE (A) Intramedullary : Oligodendroglioma, Ependymoma (B) Extramedullary : • Intradural : Meningioma, Neurofibroma, Arachnoid cyst etc. • Extradural : Neoplasm, Epidural abscess., Epidural hemorrhage, Spondylosis, Herniated disk, Post traumatic compression by fractured or displaced vertebra, or haemorrhage
- 17. Compressive v/s Noncompressive Myelopathy
- 18.
- 20. 2. NON COMPRESSIVE: A. VASCULAR • Spinal cord infraction • Arteriovenous malformation and dural fistula • Antiphospholipid antibody and other hypercoagulable states B. INFLAMMATORY AND IMMUNE MEDIATED • Multiple Sclerosis • Neuromyelitis optica • Sarcoidosis • Sjögren related myelopathy • SLE related myelopathy • Vasculitis
- 21. C. INFECTIOUS Viral :VZV, HSV-1 and 2, CMV,EBV, HIV, HTLV-1. Bacterial and mycobacterial: Borrelia, Listeria, syphillis, Mycoplasma pneumonia. Parasitic : schistosomiasis, toxoplasmosis, cysticercosis D. DEVELOPMENTAL Meningomyelocele Tethered cord syndrome E.METABOLIC Vitamin B12 deficiency (Subacute combined degeneration) Folate deficiency Copper deficiency
- 22. Causes of flaccidparaplegia (LMN type lesion) : (A) UMN LESION IN SHOCK STAGE— sudden onset spastic paraplegia in 'neural shock’ stage e.g: acute transverse myelitis, spinal injury. (B) LESION INVOLVING ANTERIOR HORN CELLS a) Acute anterior poliomyelitis. b) Progressive muscular atrophy (variety of MND). c) Trauma. (C) DISEASES AFFECTING NERVE ROOTS—Tabes dorsalis, radiculitis, G.B.S .
- 23. (D) DISEASES AFFECTINGPERIPHERAL NERVES a) Acute infective polyneuropathy (G.B. syndrome). b) High cauda equina syndrome. c) Disease of peripheral nerves involving both the lower limbs. d) Lumbar plexus injury (e.g., psoas abscess or haematoma). (E) DISEASES AFFECTING MYONEURAL JUNCTION a) Myasthenia gravis, Lambert-Eaton syndrome. b) Periodic paralysis due to hypokalaemia. (F) DISEASES AFFECTING MUSCLES Polymyositis Myopathy,myositis Muscular Dystrophy
- 24. SPECIAL PATTERNS OFSPINAL CORD DISEASES COMPLETE CORD TRANSECTION SYNDROME •All ascending tracts from below and descending tracts from above are interrupted. •All sensations are affected below the level of lesion & segmental paresthesia at level of lesion. •Quadriplegia or Paraplegia (Corticospinal tract). •Clinical effects seen in two stages Initially, spinal shock followed by hypertonic, hyper-reflexic paraplegia. •Urinary retention and constipation. • Sexual dysfunction can occur
- 25. BROWN-SEQUARD SYNDROME • Causedby hemisection injury of the spinal cord Features • Ipsilateral motor weakness (corticospinal tract) • Ipsilateral loss of joint position and vibratory sense (posterior column) • Contralateral loss of pain and temperature sense (spinothalamic tract) one or two levels below the lesion
- 26. CENTRAL CORD SYNDROME Causedby lesions in the centre of the spinal cord, such as Syringomyelia, intrinsic cord tumours etc. Features : •Arm weakness out of proportion to leg weakness •Dissociated sensory loss (Cape Distribution)
- 27. FORAMEN MAGNUM SYNDROME Weaknessof the ipsilateral shoulder and arm > weakness of the ipsilateral leg > the contralateral leg > finally the contralateral arm. This around the clock pattern of weakness may begin in any of the four limbs. Suboccipital pain spreading to the neck and shoulders
- 29. NEOPLASTIC SPINAL CORDCOMPRESSION • In adults, most neoplasms are epidural in origin • Tumours most commonly causing metastasis to the vertebral column are – breast, lung, prostate, kidney, lymphoma, and myeloma. • The thoracic spinal column is most commonly involved • Pain is the initial symptom • Glucocorticoids • Local radiotherapy and Surgery • Specific therapy for underlying tumour type
- 30. Anterior Cord Syndrome •Acuteinfraction in the territory of the anterior spinal artery produces • Paraplegia or quadriplegia • Dissociated sensory loss affecting pain and temperature sense but sparing vibration and position sense • Loss of sphincter control. •Sharp midline or radiating pain localised to the area of ischemia. •Areflexia due to spinal shock is present initially, with hyperreflexia and spasticity developing with time.
- 31. Posterior spinal arteryinfraction •Less common. •Results in loss of posterior column function
- 32. MULTIPLE SCLEROSIS • Typicallybilateral but asymmetric non compressive paraparesis • Relapsing/remitting symptoms • Autonomic symptoms causing bladder, bowel and sexual disturbances. • Episodes are “separated in time and space”. • Optic neuritis, afferent pupillary defect, ataxia, trigeminal neuralgia, recurrent facial nerve palsy Investigations : MRI and CSF Analysis
- 33. NEUROMYELITIS OPTICA • Animmune mediated demyelinating disorder • Severe myelopathy that is typically longitudinally extensive. • Associated with optic neuritis (often bilateral). • CSF studies reveal a variable mononuclear pleocytosis, and oligoclonal bands are generally absent. • Diagnostic serum autoantibodies against the water channel protein aquaporin-4 are present in 60-70%
- 34. SUBACUTE COMBINED DEGENERATION(VITAMIN B12 DEFICIENCY) • Subacute paresthesia in the hands and feet • Loss of vibration and position sense • Progressive spastic and ataxic weakness • Signs are generally symmetric • Loss of reflexes • Babinski sign positive • Optic atrophy and irritability in advanced cases
- 35. INVESTIGATIONS • Routine Investigations •X Ray of the Spine • MRI Brain • MRI Spine • CSF Analysis (Pleocytosis, oligoclonal bands etc.) • Miscellaneous : serum B12 level, autoimmune markers
- 36. Complications Of Paraplegia •Bedsores •Contractures •Urinary Tract Infection •Pneumonia •Deep venous thrombosis
- 37. REFERENCES •Harrisons principles ofInternal Medicine 21st Edition •API textbook of Medicine 12th Edition
- 38.