Heterotopic ossification

1. In what joints does HO most frequently occur in SCI?
2. How soon after injury is HO usually seen?
3. What are early clinical symptoms of HO?
4. What are risk factors for HO?
5. How is HO usually diagnosed?
6. What are treatments for HO?
7. What are possible complications of HO?

Answers:
1. 1)Hip, 2) Knee, 3) Shoulder, 4) Elbow.
2. 1-4 months post injury.
3. Heat, soft tissue swelling, decreased ROM, joint erythema/effusion, low grade fever.
4. Spasticity, complete injury, trauma to joint, age, pressure ulcer near joint.
5. Bone scan shows HO one week from onset, can be seen 7-10 days later on plain film. Elevated alk phos is also seen, but is nonspecific.
6. Treat with etidronate 20mg/kg/day for 2 weeks, then 10mg/kg/day for 10 weeks, indomethacin, maintain ROM, surgery once HO is mature (12-18 mo post injury).
7. Peripheral nerve entrapment, loss of ROM/function, increased pressure ulcers.

Restrictive respiratory changes in SCI

1. How is the forced vital capacity affected by cervical injury?
2. What are signs of impending respiratory failure?
3. What are actions that can be taken to prevent respiratory complications?

Answers:
1. In the acute phase, it decreases due to paradoxical respirations. In the chronic phase, it improves due to spasticity.
2. Increasing RR, decreasing tidal volume, decreased FVC, decreased inspiratory force, neurological level C3 or higher, can't count to 15 slowly, VC < 1L, ABG shows incr PCO2 or decr PO2, severe atelectasis.
3. IS, monitor ABGs, monitor VC, cough assist, suctioning, chest PT, strengthen pecs, glossopharyngeal breathing, pneumobelt (compresses abdominal wall to make diaphragm rise).

Phrenic pacing in SCI

1. How does phrenic pacing work?
2. What are contraindications to phrenic pacing?
3. What are benefits of phrenic pacing?
4. What are signs of failure of phrenic pacing?
5. Why might phrenic pacing fail?

Answer:
1. The intact phrenic nerves are stimulated electrically via surgically implanted electrodes.
2. Denervated diaphragm (demonstrated by EMG), denervated anterior horn cells C3-C5, less than 6 mo post-injury (chest too flaccid), significant lung impairment.
3. Increased arterial oxygenation, longer survival, increased daily function.
4. Sharp chest pain, SOB, absence of breath, erratic pacing.
5. Diaphragmatic failure (overly aggressive pacing), infection, meds (sedatives, narcotics), upper airway obstruction, phrenic nerve damage from overstimulation or surgery.

Pulmonary complications of SCI

1. What are the 3 most frequent pulmonary complications of SCI?
2. What are factors that contribute to pulmonary dysfunction in SCI?
3. What are predisposing factors to pulmonary complications in SCI?
4. What is the leading cause of death in long-term SCI patients?
5. In which side is respiratory complications most common in hospitalized SCI patients and why?

Answers:
1. Pneumonia, atelectasis, ventilatory failure.
2. Paralysis of respiratory muscles, loss of cough, injury to chest (rib fx), direct pulmonary injury (lung contusion).
3. Age, obesity, COPD, smoking.
4. Pneumonia.
5. Left sided complications are more common because the L mainstem bronchus is at a 40-50 degree angle therefore is harder to suction and tends to retain secretions.

Musculoskeletal complications of SCI

1. What are common shoulder pathologies seen in SCI?
2. How is general shoulder pain usually treated?
3. What is the incidence of CTS in SCI patients 30 years post-injury?

Answers:
1. Impingement syndrome, overuse, DJD, rotator cuff tear, bicipital tendonitis, subacromial bursitis, capsulitis, myofascial pain, disuse, cervical radiculopathy.
2. Rest, pain meds, compensatory techniques, treat condition, posture education, weight bearing education.
3. 90%.

Metabolic complications of SCI

1. What causes hypercalciuria in a SCI patient? How long does it usually take to resolve?
2. What are symptoms of hypercalcemia?
3. How is hypercalcemia treated?
4. What are treatments for osteoporosis in the SCI patient?
5. What percentage of SCI patients show signs of insulin resistance?

Answers:
1. Hypercalciuria is caused by immobilization and decreased weight bearing, which promotes bone resorption. It usually resolves in 18 months.
2. Nausea, vomiting, dehydration, decreased renal fxn, decreased mental status, abdominal discomfort, anorexia, malaise. (Stones, bones, abdominal groans)
3. IV fluids, Lasix, mobilization, steroids, decrease Vit D, etidronate, calcitonin.
4. Weight bearing and FES cycling. Medications have not been shown to help.
5. 70%.

GI complications of SCI

1. What is the likely cause of gastroesophageal bleeding in SCI patients?
2. What is the most common cause of emergency abdominal surgery in SCI patients?
3. What complication should be suspected if an adynamic ileus does not improve?
4. What is SMA syndrome? What are the symptoms? What predisposes SCI patients to this syndrome?
5. How is SMA syndrome diagnosed and treated?

Answers:
1. Ulcers secondary to interruption of sympathetic vasoconstrictors, steroid use, or increased gastric secretion.
2. Cholecystitis.
3. Pancreatitis.
4. Superior Mesenteric Artery syndrome is when the third portion of the duodenum is compressed by the overlying SMA, resulting in obstruction. The symptoms are postprandial n/v, bloating, and abdominal pain. SCI patients are predisposed due to rapid weight loss, prolonged supine position, spinal orthosis, and hyperextension of the back (due to flaccid abdominal wall).
5. It is diagnosed by an UGI series, which demonstrates duodenal obstruction to barium flow. The treatment is to eat small frequent meals upright, lie in left lateral decubitus position after eating, and Reglan.

Acute management of bowel dysfunction in SCI

1. What bowel dysfunction is a patient at risk for development in the acute period?
2. What is the usual time course of ileus in an SCI patient?
3. How is gastric atony usually managed?

Answer:
1. Gastric atony and ileus, resulting from spinal shock and reflex depression.
2. Ileus starts at 24-48 hrs and lasts from 3-7 days.
3. NG suction, IV fluids, abdominal massage to stimulate peristalsis, neostigmine injections, clear liquid diet when bowel sounds appear, Reglan.

Defecation in SCI

1. How is the bowel affected in an UMN lesion?
2. How is the bowel affected in a LMN lesion?
3. How is the gastrocolic reflex utilized in SCI?
4. How is the anorectal reflex utilized in SCI?

Answer:
1. This creates a hyperreflexic bowel with decreased ability to sense urge to defecate. External anal sphincter cannot be voluntarily relaxed but the stool can be propelled by reflex activity.
2. This creates an areflexic bowel in which reflex defecation is absent and there is slow movement of stool, resulting in constipation.
3. Increased colonic activity occurs 30-60 min after a meal, so place patient on commode within one hour of a meal.
4. Suppositories and digital stim cause the bowel wall to stretch, resulting in relaxation of the internal anal sphincter.

Innervation of the bowel

1. What is the role of the parasympathetic system in the bowel? Where does it originate?
2. What is the role of the sympathetic system in the bowel?
3. What is the role of the somatic nervous system in the bowel?
4. What takes place to allow fecal storage in a neurologically intact person?
5. What occurs during defecation in a neurologically intact person?

Answers:
1. The parasympathetic system increases upper GI motility and enhances colonic motility, via the vagus nerve and the splanchnic nerves (S2-4).
2. Sympathetic system inhibits colonic contractions and relaxes the internal anal sphincter for storage, via the hypogastric nerve.
3. Increases external anal sphincter tone for continence, via the pudendal nerve (S2-4)
4. Internal anal sphincter is sympathetically activated and relaxes, the external anal sphincter tone increases secondary to s.c. reflexes and higher cortical control.
5. Rectosigmoid distention --> reflex internal anal sphincter relaxation --> signal sent to pontine defecation center --> voluntary contraction of levator ani muscle and relaxation of external anal canal, reflexive rectal propulsions.

Infertility in SCI

1. What are causes of poor semen quality in SCI?
2. What is the most common finding noted on biopsy in men with SCI?
3. When does menstruation usually return in female patients post-SCI?
4. What are the increased risks in pregnancy with SCI?
5. What is the level of uterine innervation?

Answers:
1. Prostatic fluid stasis (improves with ejaculation), testicular hyperthermia (due to seated position), recurrent UTI, abnormal testicular histology, hormonal abnormalities, sperm antibodies, bladder management problems, medications.
2. Atrophy of seminiferous tubules.
3. 6 months.
4. UTI, leg edema, autonomic dysreflexia, constipation, thromboembolism, premature birth.
5. T10-12. If injury is above this level, the patient may not be able to perceive contractions.

Erectile and ejaculatory dysfunction in SCI

1. How do reflexogenic erections occur?
2. What are methods used to induce erections in SCI?
3. What sort of SCI provides the best chance of having the ability to ejaculate?
4. What are methods used to induce ejaculation?
5. What percentage of patients have return of sexual function within 1 year?

Answers:
1. Manual stimulation of the genital region, mediated by sacral roots S2-4
2. Medications (sildenafil), intracavernosal injection therapy, penile vacuum device, transurethral devices (alprostadil), and penile implants.
3. Incomplete LMN lesion.
4. Intrathecal neostigmine, SQ physiostigmine, direct aspiration of sperm from vas deferens, vibratory stimulation, electroejaculation (very painful if sensation intact), direct stimulation of hypogastric nerve (surgical, very painful if sensation intact).
5. 80%.

Physiology of Sex

1. What part of the autonomic nervous system controls erection and ejaculation?
2. What are the afferent and efferent limbs of the erection reflex?
3. What is the role of nitric oxide?
4. Where do the sympathetic nerves regulating ejaculation originate?
5. What is the effect of parasympathetic nerves in causing female stimulation?

Answers:
1. Erection is controlled by the parasympathetics, ejaculation by the sympathetics.
2. The afferent limb is somatic fibers from the genitals through the pudendal nerve into the spinal cord. The efferent limb is parasympathetic fibers that start in the sacral spinal cord and travel through the cauda equina and exit through S2-4 nerve roots, secreting nitric oxide.
3. Nitric oxide causes relaxation of smooth muscle of corpus cavernosum and increases blood flow to the penile arteries.
4. Fibers originate in T12-L2 and travel through the hypogastric plexus.
5. Dilation of arteries to perineal muscles and tightening of the introitus, secretion of mucus by Bartholin's glands.

Management of UTI in SCI

1. What is the WBC cutoff for treatment (per high power field) in an asymptomatic patient with SCI? What are the exceptions to this rule?
2. What are the most common urinary tract complications in neurogenic bladder?
3. What is the best way to reduce complications?
4. What are some modalities used to reduce UTIs in SCI patients?

Answers:
1. Less than 50 WBC per HPF is not generally treated and in general, asymptomatic UTI in patients with indwelling catheters in not treated. The exception is if there is vesicoureteral reflux, hydronephrosis, or growth of urea-splitting organisms.
2. Early, there is thickened bladder, later there is reflux leading to pyelonephritis and renal stones. Hydronephrosis and hydroureter is caused by outlet obstruction. There is an overdistended areflexic bladder with markedly reduced compliance.
3. Draining bladder at pressure <40mmHg.
4. Prophylactic antibiotics (unproven), Vit C supp, cranberry juice, methenamine salts.

Combination type bladder

1. What percentage of patients with SCI develop detrusor sphincter dyssynergia?
2. What sort of lesion results in DSD?
3. What is the appearance of a DSD bladder?
4. What is the consequence of untreated DSD?
5. How is DSD treated?

Answers:
1. 85%
2. Any lesion between the pontine micturition center and the sacral micturition center (S2-S4).
3. Small, tight bladder, and tight sphincter.
4. Infected urine may travel toward kidneys.
5. Anticholinergic meds to expand the detrusor, ICP, antimuscarinic drugs to cause bladder relaxation, alpha-blocker to open bladder neck, sphincterotomy.

Upper motor neuron bladder

1. What are the causes of UMN bladder?
2. Where is a lesion located that results in an UMN bladder?
3. What is the appearance of a UMN bladder?
4. What are the treatments for UMN bladder?

Answers:
1. SCI (after reflexes return), CVA, MS.
2. Above the sacral micturition center (above S2).
3. Small, hyperreflexic, overactive, little bladder, resulting in failure to store urine.
4. Ditropan (directly relaxes smooth muscle), anticholinergics, alpha-agonists, beta-agonists.

Lower motor neuron bladder

1. What are the causes of LMN bladder?
2. Where would a lesion cause LMN bladder?
3. What is the appearance of a LMN bladder and sphincter?
4. What are treatments for LMN bladder?

Answers:
1. Spinal shock, conus medullaris syndrome, cauda equina syndrome, tabes dorsalis, pernicious anemia, syringomyelia, MS.
2. Destruction of the sacral micturition center (S2-S4) or an exclusively peripheral lesion of the bladder nerves.
3. Large, hypotonic bladder with a tight competent sphincter, resulting in failure to empty. Voiding occurs when bladder can no longer expand (overflow voiding).
4. ICP, Crede maneuver (suprapubic pressure), Valsalva maneuver, cholinergic agonists, alpha-blockers.

Cystometrogram

1. What is measured during cystometry?
2. What sensations are measured during cystometry?
3. What is the accepted normal bladder capacity?
4. In a spinal cord injured patient, what should the volumes of the bladder be maintained below? What occurs if volumes are too high?
5. What are urodynamic studies performed to assess?

Answers:
1. Sensation, capacity, and presence of involuntary detrusor activity.
2. First sensation of bladder filling (100-200cc), bladder fullness (300-400cc), and urgency (400-500cc).
3. 300-600cc.
4. Volume should be maintained below 400-500cc. If higher, this can result in vesicoureteral reflux, overflow incontinence, and hydro-ureter.
5. The bladder neck, the external sphincter, and the detrusor.

Storage and emptying of the bladder

1. How do alpha-adrenergic receptors respond to NE? Beta receptors?
2. What is the innervation of the internal urethral sphincter?
3. What is the innervation of the external urethral sphincter?
4. What is the job of alpha-1 adrenergic receptors in bladder storage? What is the job of B2 adrenergic receptors in bladder storage?
5. What is the job of M2 muscarinic cholinergic receptors in bladder emptying? What is the role of B2 adrenergic receptors in bladder emptying?

Answers:
1. Alpha responds with contraction, beta responds with relaxation.
2. T11-T12 sympathetic nerve.
3. S2-S4 pudendal nerve, under voluntary control.
4. Alpha-1 receptors close the internal spincter and detrusor outlet, promoting bladder storage. B2 receptors are located in the body of the bladder and result in relaxation of the body of the bladder to allow for storage.
5. M2 receptors allow for contraction of the bladder and emptying. B2 receptors in the bladder neck relax, allowing for voiding.

Innervation of the bladder

1. What is the role of the frontal lobe in voiding? The pontine micturition center?
2. What nerves are responsible for allowing contraction of the bladder and emptying?
3. What nerves are responsible for urine storage?
4. What nerve is responsible for prevention of urine leakage and emptying?
5. Where are M2 cholinergic muscarinic receptors located? Where are beta-2 adrenergic receptors concentrated? Alpha-adrenergic receptors?

Answers:
1. The corticopontine mesencephalic nuclei of the frontal lobe inhibits the parasympathetic sacral micturition center, allowing for bladder storage. The pons coordinates bladder contraction and sphincter opening.
2. The parasympathetic efferents S2-4, traveling through the pelvic nerve.
3. The sympathetic efferents T11-L2, traveling through the hypogastric plexi.
4. The pudendal nerve, containing somatic efferents S2-S4.
5. M2 receptors are located in the bladder wall, trigone, bladder neck, and urethra. Beta-2 receptors are in the body of the bladder and neck. Alpha-adrenergic receptors are in the base of the bladder (neck and proximal urethra).

More pathology of cervical SCI

1. What is the result of a flexion injury? How does it appear on X-ray? How is the spinal cord affected?
2. What is the most common level of injury and why?
3. How do hyperextension injuries usually occur? What is the type of SCI that results? What is seen on X-ray?
4. What is the most common level of injury?
5. What is the origin of most spinal cord tumors?
6. Where do spinal cord tumors usually occur? What part of the cord is compressed?

Answers:
1. Flexion injury results in dislocation of both facets and is an unstable injury. On X-ray, there is >50% displacement of the vertebral body. The spinal cord is greatly compromised, resulting in a likely complete injury.
2. C5-C6, because there is increased movement in this area.
3. Hyperextension usually occurs through acceleration/deceleration injuries, such as an MVA. This results in disruption of the anterior longitudinal ligament (stable) and central cord syndrome, which has more UE involvement than LE. X-ray shows possible soft tissue injury.
4. C4-C5.
5. Most s.c. tumors are metastatic and are extradural in origin (involve the vertebral bodies).
6. 70% occur in the thoracic spine, compressing the anterior aspect of the spinal cord.

Cervical spinal cord injury

1. How do compression fractures usually occur? How does it appear on X-rays?
2. What is the most common level of cervical compression?
3. What is the pathology that results from a flexion-rotation injury? Is this a stable injury? How does it appear on X-ray?
4. What is the most common level of flexion-rotation injury?

Answers:
1. Slight flexion of the neck with axial loading, causing rupture of the plates of the vertebra and shattering of the body. Stable ligaments remain intact. On X-rays, it looks wedge-shaped.
2. C5.
3. Unilateral facet joint dislocation with mainly disruption of the ligaments is caused by flexion-rotation, resulting in an unstable injury (if the posterior ligament is disrupted). On X-ray, there is <50% displacement of the vertebral body.
4. C5-C6.

Spinal cord blood supply

1. What arteries provide blood to the posterior 1/3 of the spinal cord?
2. What arteries provide blood to the anterior 2/3 of the spinal cord? From what arteries do they arise?
3. What arteries serve as reinforcement for the spinal arteries?
4. What is the major source of blood to the lower anterior 2/3 of the spinal cord?

Answers:
1. Posterior spinal arteries.
2. Anterior spinal arteries, which arise from the vertebral arteries and unite to form a single artery.
3. The radicular arteries.
4. The artery of Adamkiewicz.

Ascending and Descending spinal cord pathways

1. What spinal cord tracts cross at the brainstem?
2. Which spinal cord tracts cross in the spinal cord?
3. Which spinal cord tracts remain ipsilateral?

Answers:
1. The tracts that cross at the brainstem include the corticospinal tracts (motor) and the dorsal columns (proprioception, light touch, vibration).
2. The tract that crosses in the spinal cord is the spinothalamic tract (pain, temperature).
3. The spinocerebellar tract (unconscious proprioception) remains ipsilateral.

Long tracts of the spinal cord

1. What tract of the spinal cord is responsible for proprioception, light touch, and vibration sense?
2. What tract is responsible for muscular position and tone and unconscious proprioception?
3. What tract is responsible for tactile sensation of crude touch and pressure?
4. What tract is responsible for pain and thermal sensation?
5. What tract is responsible for motor function of the arms and legs?
6. What tract is responsible for motor function of the neck and trunk?

Answers:
1. The fasciculus gracile (legs) and the fasciculus cuneate (arms), making up the dorsal columns.
2. Spinocerebellar
3. Ventral spinothalamic tract.
4. Lateral spinothalamic tract.
5. Lateral corticospinal tract.
6. Anterior corticospinal tract.

Spinal cord injury epidemiology

1. What is the prevalence and incidence of SCI?
2. What is the most common cause of SCI? What is the most common cause in the elderly?
3. What is the most common level of tetraplegia? Paraplegia?
4. What are the demographics of SCI in terms of marital status, education, and employment?

Answers:
1. 10,000 new cases of SCI per year, prevalence is 200-250,000 cases.
2. MVAs in the general population, falls in the elderly.
3. C5 tetraplegia, T12 paraplegia.
4. SCI patients are more liely to be unemployed, single, and have fewer years of education.