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Chronic Spinal Cord Injury (Lesi Medula Spinalis Khronis). Darwin Amir Bgn Ilmu Penyakit Saraf Fakultas Kedokteran Universitas Andalas. The Spinal Cord. Cervical spinal erves. Thoracic spinal nerves. Conus medullaris. Cauda equina. Lumbar spinal nerves. Sacral spinal nerves.
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Chronic Spinal Cord Injury (Lesi Medula Spinalis Khronis) Darwin Amir Bgn Ilmu Penyakit Saraf Fakultas Kedokteran Universitas Andalas
The Spinal Cord Cervical spinal erves Thoracic spinal nerves Conusmedullaris Caudaequina Lumbar spinal nerves Sacral spinal nerves
Ascending Spinal Cord Tract Conducts sensory impulses upward through 3 successive chains of neurons • 1st order neuron-cutaneousreceptors of skin and proprioceptors spinal cord or brain stem • 2ndorder neuron- to thalamus or cerebellum • 3rdorder neuron- to somatosensory cortex of cerebrum
vertebra spinal cord spinal nerve The Spinal Cord
White matter: • Myelinated axons forming nerve tracts • Fissure and sulcus • Three columns: • Ventral • Dorsal • Lateral • Gray matter: • Neuron cell cell bodies, dendrites, axons • ‘Horns’: • Posterior (dorsal) • Anterior (ventral) • Lateral • Commissures: • Gray: Central canal • White (see later for white matter pathways) Cross Section of Spinal Cord
The Spinal Cord-part of the CNS found within the Spinalcolumn The spinal cord communicates with the sense organs and muscles below the level of the head Bell-Magendie Law-the entering dorsal roots carry sensoryinformation and the exiting ventral roots carry motorinformation to the muscles and Glands Dorsal Root Ganglia-clusters of neurons outside the spinal cord The Nervous System
sensory pathway motor pathway Nerve Pathways into the Spinal Cord
Must be mastering in mind • Start by understanding anatomy and physiology of the Nervous System • Don’s forget the of CNS systematically • - Anatomy of CNS • - Physiology of CNS • - Pathophysiology of the Disease • - The steps to make the diagnosis Symptoms and Signs
▪Soft touch, pain, temperature, position, vibration impaired below the level of lesion ▪Band like radicular pain/segmental paraesthesia at the level of lesion ▪localised vertebral spine pain- destructive lesions Sensory disturbances
▪ Paraplegia/quadriplegia ▪ Acute-flaccid/ Areflexic-spinal shock latter-hypertonic/hyper reflexic, loss of superficialreflexes, Babinski +, flexor/extensor spasm ▪ Extension of hip, knee occurs in high spinal & Incomplete lesion Motor disturbances
•Flexion of hip , knee occur in low spinal & complete lesion •At the level of lesion – paresis, atrophy, fasciculations,andareflexia(LMN signs) in a segmental distribution because of damage to the anterior horn cells and ventral roots Motor disturbances
initially atonic, latter spastic bladder, rectal sphincter disturbances • orthostatic hypotension • trophic skin changes • anhydrosis • impaired temperature control • vasomotor instability • sexual disturbances • I/L horner syndrome Autononomic disturbances
Causes of Chronic Lesion ° Tumour ° Multiple sclerosis ° Vascular disorders ° Spinal epidural hematoma/abscess ° Auto immune disease ° Herniatedintervertebral disc ° Combine degeneration of B12 Deficiences
Complete spinal cord transection(Transverse myelopathy) • All acsending tracts from below the level of the lesion and all descending tract from above the level of lesion interrupted.Motor, sensory, autonomic functions below the level of lesion disturbed • Causes : °tumour° multiple sclerosis ° vascular disorders° spinal epiduralhematoma/ ° spinal epidural abscess °herniated intervertebral disc ° auto immune disease
Central spinal cord lesion • Spinal cord damage starts centrally and spreads centrifugally • Decussating fibers of spinothalamic tract involved initially • Thermo anaesthesia, analgesia in a ”vest like” or “suspended” bilateral distribution with preservation soft touch sensation and proprioception--- dissociation of sensory loss
Forward extension of diseaseanterior horn cells involved segmental neurogenic atrophy, paresis, areflexia • Lateral extension I/L Horner syndrome Kypho scoliosis Spastic paralysis • Dorsal extension I/L Position sense, vibratory loss Central spinal cord lesion
Extreme venterolateral extension thermo anaesthesia, analgesia with sacral sparing • Neuropathic arthropathy • Pain Central spinal cord lesion
Tabesdorsalis-tabeticneuro syphilis, progressive locomotor ataxia • Impaired vibration and position sense, and decreased tactile localisation • Lability of mechanical sensation threshold, tactile & postural hallucinations, persistence of mechano receptor sensation, disturbances in the knowledge of extremity movement and positions(temporal & spatial disturbances) • Sensory ataxia in dark, Romberg(+) Posterior column disease
Posterior column disease • Ataxic / stomping/ double tapping gait • Positive sink sign • In tabesdorsalislancinating pain, urinary incontinence, Negative patellar and ankle DTR, hypotonic limb, hyper extensible joints abdominal, laryngeal crises, impaired light touch perception, Argyll robertson pupil, optic atrophy, ptosis, ophthalmoplegia
Posterior column disease ○Lhermitte sign or barber chair syndrome due to increased mechano sensitivity ○Truncal and gait ataxia : also seen inmets causing cord compression ○ Impaired conduction in dorsal spinocere -bellar tractmay be a primarmanifestation of epidural spinal cord compression-lower extremity dysmetria and gait ataxia. ○ Pt usually have thoracic spine compression due to selective vulnerability of spinocerebellar tract in thoracic spine to compres -sive ischemia
Hemisection of the spinal cord( Brown sequard syndrome) • Loss of pain, temp C/L to the hemisection- interruption of crossed spino thalamic tract • Loss of proprioception – interruption of ascending fibers of posterior column • Spastic weakness due to interruption of descending cortico spinal tract • Segmental LMN signs and sensory changes at the level of lesion due to damage of the roots and anterior horn cells at the level of lesion
Thank you Brain For all you remember What you forgot was my fault
The End TERIMA KASIH