Clinical Neuroscience Assignment- Option 1
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
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
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.
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
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).
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).
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