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Clinical Neuroscience Assignment- Option 1 Introduction:
For the purpose of this report, the interviewee has been given a pseudonym of Michael. The condition to be discussed is traumatic spinal cord injury (SCI). The report will include diagnosis; clinical manifestations; diagnostic procedures; treatment/management; future strategies and the pathophysiology of the condition. Carlson & Gorden (2002) propose that “acute traumatic SCI represents one of the most devastating injuries to afflict the human body” (pg. 116). The injury has a high prevalence among the younger population; especially males aged 16-30 years. Approximately 10,000 new cases are reported each year. Typical causes include motor vehicle accidents, violence, falls and recreational activities (McDonald & Sadowsky, 2002). On 1/10/2007, Michael aged 20 years, dove into shallow beach water and endured a SCI resulting from vertical compression. In early stages of hospitalisation, Michael was diagnosed with a C5 complete SCI secondary to C6 and C7 vertebral fractures. On discharge, Michael‟s neurological level was identified to be a C6 complete SCI. Parker (2003) states that diagnosis may change after some time as spinal shock makes the initial diagnosis difficult due to the inflammation and trauma at the injury site. The importance of diagnosis in relation to traumatic SCI is to isolate the injury, determine the magnitude and effect of the injury and to prevent further damage from occurring. Secondary to this is to implement management strategies that will improve the client‟s condition so they can return to a „normal‟ life; with assistive technology if necessary (Somers, 2001). Chronology of complaints:
The initial compression force of striking the head on the sand bank resulted in instantaneous, complete loss of mobility and sensation from the lesion level down. The symptom experienced is spinal shock which occurs immediately after injury (Somers, 2001). Other signs and symptoms experienced by Michael include neurogenic shock; autonomic dysreflexia; flaccid paralysis of muscles at lesion level; and spastic paralysis of muscles below the lesion level. Michael had also lost reflexes and sensation below the level of injury as well as sexual function and bowel and bladder control. Due to the nature of SCI‟s the onset of the signs and symptoms are acute and develop directly after injury due to disruption of the ascending and descending tracts within the spinal cord According to Nelsen-Marsh (2005), Michael experienced common signs and symptoms of a C6 SCI. The most distinctive symptom is spinal shock. The clinical manifestations experienced at and below the level of injury include flaccid paralysis of muscles; loss of spinal reflexes; loss of sensation (vibration, touch, pain, temperature and proprioception); loss bowel and bladder control with paralytic ileus; loss of sexual function and loss of thermoregulation. Dry and pale skin is also a common feature (Boss, 2006; Lombardo, 2003; Neurogenic shock (a form of spinal shock) was also experienced. Signs and symptoms such as altered vasomotor response, hypotension, bradycardia, unstable blood pressure and inability to perspire occurred below level of injury (Braun & Anderson, 2007). Post spinal shock, Michael reports having increased tone (spasticity) and spasms in his lower Michael has normal function above the level of injury. For a C6 lesion, this includes full head, neck, diaphragm, shoulder and upper arm function in addition to some forearm function. However, the distal extremities (wrists and digits) are not as functional (Porth, 2007). Michael has impaired sensation on the underside of his upper arm and the ulnar side of the forearm and hand. Michael had also endured some pressure sores on his elbows (bilaterally) due to prolonged, unrelieved pressure (Somers, 2001). Overall, he has nil movement and sensation from the nipple line down. Whilst in hospital (6 months in total), Michael had experienced a few episodes of autonomic dysreflexia. He reported a pounding headache and a rash on his neck. He had also noticed that his catheter was pulled half-way out. Other common signs of autonomic dysreflexia are sudden episodes of hypertension, bradycardia, piloerection (goose-bumps), upper body sweating and flushing and lower body vasoconstriction (Nelsen-Marsh, 2005). To date, Michael still reports having nil sensation and voluntary control below the lesion level. However, his symptoms are managed by medications, physiotherapy and occupational therapy. Michael currently has less spasticity and spasms in muscles below the level of Diagnostic Procedures:
On admission to the emergency department (ED), a neurological evaluation was conducted to assess Michael‟s level of consciousness, cranial nerve function, voluntary motor function and reflexes. The evaluation and testing Michael experienced on arrival to the ED was typical for a SCI patient, as baseline data that is collected is further used to make decisions regarding future management and evaluation (Somers, 2001). Harrop, Sharan & Ratliff (2006) and Somers (2001) propose that radiologic investigation is essential to determine the extent to which the spinal column, cord, and associated structures are compromised as well as possible treatment options. Recent advances in medical imaging have enabled further visualisation and insight into the etiology and pathogenesis of SCI‟s. Standard x-rays are performed initially to examine the injury whilst the spine is immobilised (Somers, 2001). Michael‟s x-rays showed a fractured C7 vertebra. For cervical SCI‟s, imaging should cover a lateral view encompassing C1 through to the C7/ T1 junction as well as an anteroposterior view (Kaji & Hockberger, 2007; Parker, 2003; Somers, 2001). Computed tomography (CT) scans and magnetic resonance imaging (MRI‟s) were also performed. The CT scan provided more detailed images that revealed fractures not evident in x-rays. The MRI showed detailed imaging of morphological changes in soft tissue, ligaments and intervertebral discs as well as the degree of spinal instability (Harrop et al., 2006; Kaji & Hockberger, 2007). Other diagnostic procedures used include urodynamics (for urinary tract) which showed detrusor hyperreflexia with loss of sensation as well as a cystoscopy (looking at the urinary bladder via the urethra) of which the results were unremarkable. Collectively, the above diagnostic procedures presented indications for surgery due to the fractured vertebrae (C7) and evident fractures (C5, 6). The unstable cervical spine could lead to further compression and damage of the spinal cord and associated neural elements Management:
At the trauma site, Michael was fitted with a neck brace and his body was stabilised with a backboard to avoid movement and further damage. This was an appropriate form of initial treatment according to Porth (2007). He was then flown to the hospital. On admission to the emergency department, the primary management was centred on assessing Michael‟s neurological function. Three hours post injury, Michael was administered Methylprednisoline (a high-dose steroid) to prevent further damage and increase neural outcomes (Somers, 2001; Michael‟s management was provided by a multidisciplinary team. The team included specialists, general practitioners, nurses, a nurse educator, physiotherapist, occupational Michael‟s hospitalisation consisted of admission into emergency (1 day); he then was moved to the high dependency unit prior to surgery (1 day); post surgery, he was sent to the intensive care unit (7 days) and then transferred to the acute spinal unit (for 6 weeks). For the remainder of his hospitalisation, Michael was placed into the spinal rehabilitation unit. Michael began his medication and bowel and bladder management immediately. Occupational therapy (OT) and physiotherapy commenced once Michael was transferred to the acute spinal unit. The rehabilitation provided started at a slow and steady pace; increasing Carlson & Gorden (2002), Lombardo (2003); McDonald & Sadowsky (2002), Somers (2001) and Winter & Pattani (2008) support the following treatment options. All diagnostic procedures required (as stated above) were carried out and a decision was made to perform surgery as early as possible to stabilise the spine. The surgery was carried out 72 hours post injury. The surgery performed was a cervical fusion (anteriorly). The internal fixation of C7 occurred via a bone graft. Bone was harvested from the patient‟s right iliac crest. Finally, C5, 6 and 7 were fused together with a titanium rod (spinal instrumentation). The effect of surgery was successful in stabilising the spine as well as decreasing hospitalisation time and functional deterioration. Post surgery, Michael was intubated for 5 days. Within this time, some congestion developed on the lungs. Michael‟s respiratory management included cough and decongestant medications. During this time, he also had visits from the physiotherapist who taught him deep breathing exercises and assisted cough techniques. Treatment for spinal shock centred on maintaining normal hemodynamic parameters with insistent fluid resuscitation; vasopressors and continuous monitoring of heart rate and urine Whilst in the hospital, Michael‟s bladder management involved a suprapubic catheter (SPC) insitu (changed monthly) in addition to Ditropan. On discharge he was provided with Oxybutynin (5mg) to relieve urinary and bladder difficulties. Bowel management during hospitalisation included daily AM Microlax enemas, Normacol Plus, Metamucil and Coloxyl (120mg) to assist bowel movements. Upon discharge, he was advised to maintain the above medications. Skin/wound management included patient education, a quad inspection mirror and pressure cushions/mattress. During hospitalisation, the OT also taught Michael how to transfer between 2 surfaces to relieve pressure. These strategies decrease the development of pressure Physiotherapy during hospitalisation included stretches for increased muscle tone, spasms and shortened tendons. Rehabilitation was also required to strengthen muscles (especially upper limbs and trunk) and decrease atrophy. The physiotherapist also provided fluid (respiratory) management as mentioned above. During OT, hand and calf splints were provided but were not maintained as no significant effect was evident. The therapist also provided functional training in relation to self-care, wheelchair use, other equipment required, transfers, mobility and balance. Prior to discharge, a wheelchair safety check was conducted and modifications were made to the van and family Michael reports having gained greater movement and sensation in his hands and wrists. Medications provided during hospitalisation (in addition to the medications stated above) included pain killers, muscle relaxants, fibre tablets and stomach/antacid tablets. He was also administered Anginine tablets for management of autonomic dysreflexia. Upon discharge, Michael was also advised to take Multivitamins and Anginine tablets (as needed). The above management strategies were implemented to limit secondary injury, alleviate clinical manifestations and to improve quality of life and functional status (McDonald & Currently, Michael is living at home and is maintaining his medications, physiotherapy and OT (2 per discipline per month). He also meets with a community nurse once a month for follow-ups and has joined community services such as Burn Rubber Burn and Spinal Outreach. Michael currently has full arm and wrist range of motion (bilaterally). He still has some difficulty with hand function (grasp and finger movement) and no sensation in his 5th digits (bilaterally). OT goals are focused on increasing hand function. Future Strategies:
Once discharged from hospital, Michael was advised to continue physiotherapy and OT in the community. By doing so, he would maintain and increase motor and sensory function. He was also to continue taking his medications for bowel and bladder management. Michael is also required to attend hospital follow-ups every year. Medical imaging required includes MRI‟s and intravenous pyelography‟s (IVP‟s) once per year to monitor his neurological status. Michael has been advised to visit his local medical officer for prescription referrals and regular blood tests. Future goals for Michael are to return to work and obtain a licence to drive a specialised car. To do so, he will need to consult with his OT. Michael reports that his life has changed so drastically since the incident. He now requires assistance (a carer) to help him within the home. Michael wishes to be more independent over time. Sarhan & Cummings (2008) suggest that future management strategies should encompass ongoing assessment especially in relation to the general health of the patient. They also suggest the use of fitness and nutrition programmes; positive health behaviours and health promotion services. Comprehensive history, physical examination, assessment of spinal cord injury functional level and an evaluation of general health-related risk factors should be conducted every few months. Men in particular should also be screened for prostate cancer and have digital rectal examinations. Respiratory assessments (forced vital capacity and forced expiratory volume in 1 second) as well as urological evaluations are also Pathophysiology:
SCI‟s essentially disrupt both upper and lower motor neurons. Therefore both ascending and descending spinal cord tracts are disrupted leading to the blockage of signals at the level of injury (McDonald & Sadowsky, 2008). Ascending (sensory) tracts include the dorsal column/medial lemnsicus pathway which carries discriminative touch and conscious proprioception to higher centres; spinothalamic tracts which carry discriminative pain, temperature and coarse touch; divergent pathways which carry localised pain and spinocerebellar tracts which carry movement related information from the periphery (Lundy- Ekman, 2002). Descending (motor) tracts include corticospinal tracts; reticulospinal tracts, tectospinal tracts, rubrospinal tracts, vestibulospinal tracts as well as raphespinal and cerulospinal tracts which carry pain transmission (Lundy-Ekman, 2002). The pathophysioloic process of traumatic SCI can be divided into two types: primary and secondary. The primary neurologic injury is the irreversible damage that occurs at the time of mechanical injury. Primary injury is often characterised by small haemorrhages of the grey matter as well as oedematous changes in the white matter. This leads to neural tissue necrosis (Porth, 2007). The mechanism of injury in this report is vertical compression which results in burst fractures. Neurological damage occurs when bony vertebral fragments compress the cord or are driven posteriorly into the spinal canal (Somers, 2001). Secondary injuries follow the primary injury and amplify the spread of injury thus leading to progressive neurologic damage (Porth, 2007). Somers (2001) proposes that most damage is caused by secondary Immediately after traumatic injury to the spinal cord, functions of the cord below the level of the lesion are lost or depressed. This temporary condition, known as spinal shock, is caused by disturbance to descending tracts that deliver tonic facilitation to spinal cord neurons (Lundy-Ekman, 2002). As the lesion occurred at C6, the phrenic nerve was not involved therefore the patient has uncompromised breathing. However, respiratory congestion may occur due ineffective coughing which allows a build-up of secretions to form in the lungs The pathophysioloic process of spinal shock is poorly defined. Although, it is evident that during spinal shock; autonomic, reflexive, motor and sensory activity is lost below the level of injury (Braun & Anderson, 2007). McDonald and Sadowsky (2008) discuss the role of hypo-perfusion that develops post injury in the grey matter. Hypo-perfusion contributes to spinal shock as it slows/blocks propagation of action potentials along the axon. McDonald & Sadowsky (2008) also suggest that damaged cells, axons and blood vessels release toxic chemicals which attack nearby, functional cells therefore resulting in progressive secondary injury. Somers (2001) proposes that secondary tissue destruction can result from ischemia, inflammation, ion derangement and accumulation of calcium inside injured cells. Gould (2002) and Lombardo (2003) suggest that during spinal shock all function is normal above the level of trauma and inflammation and no sensory or motor impulses are seen below the lesion level. Common features include flaccid paralysis (due to lower motor neuron damage); loss of withdrawal and deep tendon reflexes; loss of smooth muscle tone and reflexive emptying of the bowels and bladder (urinary retention and paralytic ileus) as well as loss of autonomic regulation of blood pressure and thermoregulation (Lundy-Ekman, 2002). Lundy-Ekman (2002) also suggests that poor thermoregulation can interfere with the body‟s ability to maintain homeostasis. Therefore the interruption may result in excessive sweating above the level of injury to compensate for the loss. Hypothermia is also a risk as the patient does not have the ability to shiver below the injury level. Post spinal shock, all function is normal above the level of injury and no sensation and voluntary movement is seen below the level of injury. Spastic paralysis (due to upper neuron damage) occurs in the trunk and legs. Bladder and bowel incontinence is also present. There is also no central control over the sympathetic nervous system (Gould, 2002). Neurogenic shock (a form of spinal shock) may also occur. Neurogenic shock results from impairment of descending sympathetic innervation to the vasculature which results in vasodilation thus initiating hypotension and bradycardia (Lombardo, 2003). Lundy-Ekman (2002) suggests that hypotension occurs due to the loss of sympathetic vasoconstriction combined with decreased muscle-pumping action for blood return. As spinal shock resolves, autonomic dysreflexia (hyperreflexia) takes place. Autonomic dysreflexia is a potentially fatal complication that occurs at or above the T6 vertebra (splanchnic outflow). Autonomic dysreflexia is triggered by noxious stimuli. Some include constipation, distended bladder, full bladder, urinary tract infections (UTI‟s) and cutaneous stimulation below the level of injury. These stimuli cause excessive sympathetic reflex activity to occur. Autonomic dysreflexia is characterised by sudden episodes of hypertension, a pounding headache, unstable blood pressure and vasoconstriction. Subsequently, parasympathetic activity produces activation of the vagus nerve (baroreceptors sense elevated blood pressure due to sustained sympathetic activity) which results in bradycardia and vasodilation above the level of injury. Profuse sweating and body flushing also occurs above the level of injury. In SCI patients, autonomic dysreflexia is a life-threatening complication as inhibiting signals descending from the brain to spinal cord neurons cannot pass below the level of lesion (Lundy-Ekman, 2002; Middleton, Leong & Mann, 2008a; Nelsen-Marsh, Bladder function is achieved by visceral afferents that convey smooth muscle stretch to the spinal cord and up to the brain. Reflexive voiding occurs when the bladder is full. This is achieved by activating parasympathetic efferents (which contract the bladder) and inhibiting somatic efferents (which relax the external sphincter). Lesions above the sacral cord interrupt the ascending and descending axons; isolating the sacral reflex centre from the higher centres. Common clinical manifestations presented are loss of voluntary control of micturition reflex and coordinated voiding and loss of bladder sensation. The bladder becomes hypertonic and hyperreflexic with reduced bladder capacity (Lundy-Ekman, 2002; Middleton, 2004). The effects of SCI on bowel function are similar to those on bladder function. Lesions above the sacral cord result in no sensory awareness and no control of sphincters. Yet reflexive emptying of the lower bowel can still be achieved via rectal stretch (reflexive lower bowel circuit is intact) (Lundy-Ekman, 2002; Stolzenhein, 2005). After SCI, changes occur in genital sensation, arousal and orgasm. Sexual function is controlled by S2-S4 (erection) and L1-L2 (ejaculation) parasympathetic fibres. Lesions above this level result in impaired sexual function. However, sexual function may be elicited by genital touch (Lundy-Ekman, 2002; Middleton, Leong & Mann, 2008b). Both neuropathic and nociceptive pain can also be experienced. The pathology of pain is poorly defined but is usually associated with inflammation, overuse, compression, trauma and ischemia (Middleton & Siddall, 2004). Conclusion:
In conclusion, Michael has endured a complete C6 SCI. He has experienced normal signs and symptoms associated with this type of lesion. These include spinal shock, autonomic dysreflexia and alterations in relation to bowel, bladder and sexual function. Appropriate treatment measures were provided and are still maintained to date. Michael wishes to gain more independence. He is currently attending driving lessons to obtain a licence for a specialised car. The role of the OT in relation to SCI is to assist the client in gaining functional independence as well as to participate socially and productively (work-related). Reference List
Boss, B.J. (2006). Alterations of neurologic functional. In K.L. McCance & S.E. Huether, Pathophysiology: the biologic basis for disease in Adults & Children (5th ed.) (pp. Braun, C.A. & Anderson, C.M. (2007). Pathophysiology: Functional alterations in human health. Baltimore: Lippincott Williams & Wilkins. Carlson, G.D., & Gorden, C. (2002). Current developments in spinal cord injury research. Gould, B.E. (2002). Pathophysiology for the health professions (2nd ed.). Philadelphia: W.B. Harrop, J.S., Sharan, A., & Ratliff, J. (2006). Central cord injury: Pathophysiology, management, and outcomes. The Spine Journal, 6, 198-206. Kaji, A., & Hockberger, R. (2007). Imaging of spinal cord injuries. Emergency Medicine Clinics of North America, 25, 735-750. Lombardo, M.C. (2003). Central nervous system injury. In S.A. Price & L.M. Wilson (Eds.), Pathophysiology: Clinical concepts of disease processes (6th ed.) (pp. 869-880). St. Lundy-Ekman, L. (2002). Neuroscience: fundamentals for rehabilitation (3rd ed.). St. Louis: McDonald, J.W., & Sadowsky, C. (2002). Spinal-cord injury. The Lancet, 359, 417-425. Middleton, J. (2004). Management of the neurogenic bladder for adults with spinal cord injuries. (NSW State Spinal Cord Injury Service, CD-ROM, 2007 release). Middleton, J.W., Leong, G., & Mann, L. (2008a). Management of spinal cord injury in general practice- Part 1. Australian Family Physician, 37(4), 229-233. Middleton, J.W., Leong, G., & Mann, L. (2008b). Management of spinal cord injury in general practice- Part 2. Australian Family Physician, 37(5), 331-338. Middleton, J., & Siddall, P. (2004). Managing pain for adults with spinal cord injuries. (NSW State Spinal Cord Injury Service, CD-ROM, 2007 release). Nelsen-Marsh, J.D. (2005). Chronic disorders of neurologic function. In L.C. Copstead & J.C. Banasik (Eds.), Pathophysiology (3rd ed.) (pp. 1124-1148). St. Louis: Elsevier Parker, S. (2003). Spinal cord and nerves: Injury, illness and health. Chicago: Heinemann Porth, C.M. (2007). Essentials of pathophysiology: concepts of altered health states (2nd ed.).
Philadelphia: Lippincott Williams & Wilkins. Sarhan, F., & Cummings, P. (2008). Health promotion for people with spinal cord injury: improving quality of life. British Journal of Neuroscience Nursing, 4(8), 374-380. Somers, M.F. (2001). Spinal cord injury: Functional rehabilitation (2nd ed.). Upper Saddle Stolzenhein, G. (2005). Management of the neuropathic bowel for adults with spinal cord injuries. (NSW State Spinal Cord Injury Service, CD-ROM, 2007 release). Winter, B., & Pattani, H. (2008). Spinal cord injury. Anaesthesia and Intensive Care

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