This document provides guidance on evaluating patients presenting with paraplegia. It outlines the key components of the clinical history and neurological examination needed to determine the cause and level of spinal cord injury. The history should ascertain details of onset and any associated symptoms. The exam focuses on assessing sensory and motor function at different dermatomal and myotomal levels to localize the lesion. Together this information can indicate if the injury is acute, subacute, or chronic, and identify potential etiologies like trauma, infection, inflammation, compression, or vascular causes. The goal is to arrive at a diagnosis and localization of injury within the spinal cord or vertebrae.
Dr Abdullah Ansari
PG-2 (Medicine)
AMU ALIGARH
A general approach to periodic paralysis....
(including hypokalemic periodic paralysis and thyrotoxic periodic paralysis, and other “Channelopathies” or “Membranopathies)
Pathophysiology
Epidemiology
Primary or familial periodic paralysis
Secondary periodic paralysis
Conventional classification of periodic paralysis
Classification of primary periodic paralysis based on ion-channel abnormalities
Clinical approach to a case of periodic paralysis
History of muscle weakness
Age of onset
Family history
Timing
Intensity
History of administration of certain drugs
Clinical examination
Differential Diagnosis
Laboratory investigations
Serum K+
CPK and serum myoglobin
ECG
EMG
Nerve conduction studies
Provocative Testing
Muscle biopsy
Treatment
Prognosis
Dr Abdullah Ansari
PG-2 (Medicine)
AMU ALIGARH
A general approach to periodic paralysis....
(including hypokalemic periodic paralysis and thyrotoxic periodic paralysis, and other “Channelopathies” or “Membranopathies)
Pathophysiology
Epidemiology
Primary or familial periodic paralysis
Secondary periodic paralysis
Conventional classification of periodic paralysis
Classification of primary periodic paralysis based on ion-channel abnormalities
Clinical approach to a case of periodic paralysis
History of muscle weakness
Age of onset
Family history
Timing
Intensity
History of administration of certain drugs
Clinical examination
Differential Diagnosis
Laboratory investigations
Serum K+
CPK and serum myoglobin
ECG
EMG
Nerve conduction studies
Provocative Testing
Muscle biopsy
Treatment
Prognosis
LOW BACK PAIN. Dr Haki Selaj Residency in Kosovo QKUKHakiSelaj1
back pain is a very widespread pathology in the world. There are health and socioeconomic consequences. widespread both in the young and in the old. The causes are different. The overwhelming majority is mechanical pain without a specific cause, while the others are pain from disc, infections, tumors, fractures, metabolic.
Cns case-extramedullary compressive myelopathy, Q&AKurian Joseph
Tracts involved-corticospinal tract
anterior and lat spinothalamic
posterior coloumn
Mostly extramedullary compressive myelopathy at T10 level
Etiology –to consider both intra and extradural causes like neurofibroma/meningioma/av malformation.
extradural-potts spine,ivdp
Approach to a patient with CNS diseaseAhsan Sajjad
Approach and management of a patient showing signs and symptoms of CNS disease. Although its an extensive Presentation but it contains all the relevant knowledge which was possible by me to Gather.
Contains 17 clinical situations of prolonged fever and discussion of various differential diagnosis based on them. Also gives the key points in the diagnosis of a prototype diagnosis and the usefulness of a relevant investigation modality in identifying these conditions. This power point presentaion is based on the chapter in Harrison's Text Book on Internal Medicine chapter on Fever of Unknown Origin
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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NYSORA Guideline
2 Case Reports of Gastric Ultrasound
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
1. Dr. S. Aswini Kumar. MD. Professor of Medicine 1 Clinical Evaluation of Paraplegia
2. Anatomy of spinal cord Cranial border of atlas 45 cm in adult male 42 cm in adult female Corresponding spinal column 70cm Lower border of L1 Total 31 segments 2
3. Structure 3 Intra medullary Extra medullaryintradural Extra medullaryextradural
9. History taking in paralplegia What is the onset of paraplegia? Is it acute – within, minutes or hours? Is it subacute – within days or weeks? Is it chronic – within months or years? Was there a history of trauma? Fall from height/road traffic accident/direct injury? Was there a history of back pain? Duration/maximum intensity/history of spinal surgery? 9
10. Any girdle pain or radicular(root) pain? Is there any girdle pain / sensation? Pain around the thorax or abdomen Is it unilateral or bilateral? Does it increase with coughing and sneezing? Is there a history of root pains? Is it unilateral or bilateral? Does it radiate to the limbs? Does it aggravate with coughing? 10
11. History suggestive of tract involvement? Any pyramidal tract involvement? Buckling of knees/Slipping of chappals/Tripping on objects? Any lower motor neuron involvement? Loss of tone, wasting and fasciulations Any dorsal column involvement? Swaying while washing face or difficulty in walking at night? Any cerebellar involvement? Any swaying while walking/inability to sit upright/incordination 11
12. History of past illnesses History of viral infections? Viral infections/Chicken pox/Herpes zoster/HSV-1&2/HIV/CMV/HTLV History of vaccination? Anti Rabies vaccination/Polio vaccination/Others? Hisory of tuberculosis? Any where in the body-Pulmonary/intestinal/lymphnodal/miliary History of Malignancy? Swellings/ surgery for tumors/Chemotherapy or radiation 12
13. Personal history Any bladder involvement? Retention /overflow incontinence/bladder sensation? Any bowel involvement? Constipation/bowel incontinence/bowel sensation? Any sexual dysfunction? Morning Erection/los of libido/sexual promiscuity? Any autonomic dysfunction Excessive sweating/absence of sweating 13
14. Complete neurological examination Optic fundi Lower cranial nerves Motor system in full Sensory system in full Superficial reflexes Deep tendon reflexes Cerebellar signs Spine 14
15. 1. Does the patient have neurological problem? Yes/no Or is it a medical condition simulating paraplegia? Fracture dislocation of pelvis/ Polyarthritis of joints of limbs Or is it a case of GullainBarre Syndrome Or is it Hysteria or malingering If Yes what is the nature of the deficit? Paraplegia/quadriplegia/ cerebral diplegia/cerbral paraplegia 15
16. 2. What is the mode of onset of paraplegia? Acute Transverse myelitis, Traumatic paraplegia, Anterior spinal artery syndrome Sub acute: Pott’s paraplegia, Spinal epidural abscess, Spinal cord tumors Chronic Familial spastic paraplegia, Amyotrophic lateral sclerosis, Cranio-vertebral junctional anomalies 16
17. 3. What are the subjective sensory symptoms? Radicular (root) pain or Girdle pain Unilateral or bilateral sharp shooting pain of dermatome distribution Exacerbated by coughing, sneezing or valsalva Vertebral pain: An aching pain confined to a point of spine accompanied by point tenderness Neoplastic or inflammatory dural lesion likely Funicular pain Deep seated ill defined dull ache distant from the affected cord level Common with intra-medullary lesion 17
18. 4. What are the objective sensory deficits? These may be in the form of Segmental hyper-aesthesia Hypesthesia (decreased touch sensation) Hypoalgesia (decreased pain sensation) Loss of all modalities below a level Loss of position and vibration sense Dissociated sensory loss Suspended segmental loss of pain and temperature Loss of pain & temperature below a particular level 18
19. 5. What are the motor deficits? Is there any muscle wasting? Is there a disuse atrophy? Is there a distal muscle wasting? Small muscle wasting in syringomyelia? Is there a proximal muscle wasting? What is the tone of the muscles? What is the distribution of motor weakness? Is there any abnormal movements? Is there any loss of co-ordination? 19
20. 6. What are the changes in superficial reflexes? Abdominal reflexes of all 4 quadrants are absent. Cremasteric reflexes absent bilaterally. Plantars are extensor bilaterally - D7 lesion Abdominal reflexes of upper quadrants are present. Lower quadrants are absent. Beever’s sign is positive. Plantar reflexes are extensor bilaterally - D10 lesion Abdominal reflexes of all four quadrants are present. Both cremasteric reflexes are absent. Plantar reflexes are extensor bilaterally. - L1 lesion 20
21. 7. What are the changes in the deep reflexes? Loss of Deep tendon reflexes at segmental level with exaggerated DTR below the level indicate level of lesion Biceps reflex – C5 Supinator reflex – C5 Inversion of supinator – C5 C6 Triceps reflex – C7 Knee reflex –L2 L3 Ankle reflex – L5 S1 21
22. 8. Is it an LMN/UMN lesion or a combination? LMN signs alone would indicate the possibility of Anterior horn cell lesion (Spinal muscular atrophy) Nerve root disease ( Radiculopathy) Peripheral nerve lesion ( Peripheral neuritis) Myoneural junction abnormality (Myasthenia) Primary Muscle disease (Myopathies) LMN signs of a segmental distribution indicates an appropriate level of lesion Bilateral UMN findings below that level indicates a transection of corticospinal tracts on either sides Both LMN and UMN signs at the same level suggests the possibility of motor neuron disease 22
23. 9. What is the segmental level of lesion? It is derived from the information gathered through collection of the data as above Sensory segmental level by root/radicular /girdle pain segmental hyperaesthesia Loss of sensations as per dermatomes Motor segmental level Superficial reflex level Deep tendon reflex level Bladder function level 23
24. 10. Are there other features of the level? Upper Cervical Cord QP and weakness of diaphragm Lesion of C5-C6 Loss of power and reflex at biceps Lesion of C7 segment Triceps, wrist extensors and fingers Lesion of C8-T1 segments Finger and wrist flexion, Horners Lesions of mid thoracic region? Sensory level at trunk, midline back pain 9th and 10th thoracic segments Paralysis of lower not upper abdomen L2 – L4 segments Flexion and abduction of thigh L5 – S1 segments: Flexion knee, extension thigh, foot S3 – S4 segments: Saddle anesthesia, bladder and bowel Caudaequina Root pains, asymmetrical leg weakness 24
25. 11. What is the vertebral level? Calculated in a reverse direction From cervical segments- subtract 1 From upper thoracic segments- subtract 2 From lower thoracic segments- subtract 3 Lumbar 1-2 segments- T10 vertebra Lumbar 3-4 segments- T11 vertebra Lumbar 5 segments- T12 vertebra Sacral and coccygeal segments 25
27. 13. What are the nuclei/tracts involved? 1. Complete transection of spinal cord 2. Hemi-section 3. Central lesion 4. Posterior and lateral column lesions 5. Posterior column disease 6. Anterior horn cell disease 7. Anterior horn cell + pyramidal 8. Plexus lesion/radiculopathy 27
28. 14. Is it a Vascular syndrome of spinal cord? Features Abrupt onset girdle pain/radicular pain Flaccid paraplegia within minutes /hours Thermo anesthesia Analgesia below the level Impaired bowel and bladder control Watershed zones C4 T4 segments L1 segment Causes: Arteriosclerosis of spinal arteries 28 abnormally increased T2 signal is seen within the central portion of the distal spinal cord
29. 15. Am I dealing with a spinal cord compression? Diseases of the vertibral column? Trauma, Tuberculosis, Secondaries of spine Primary neoplasms: Sarcoma, Myeloma, Hemangioma Infiltrations: Leukemis deposits Reticulosis Cystic lesions Spinal cord tumors 29
30. 16. Or is it a non compressive myelopathy? A. Infective: Viral – Poliomyelitis, Herpes zoster, Rabies Bacterial – Tuberculosis, Syphilis Parasitic, Falciparum Malaria and Schistosomiasis B. Immuno-allergic Post exanthematous –Measles, Rubella Post vaccinial – Rabies, Polio Transverse myelitis 30