Wheelchair cushions and operation

1. What is the benefit of having a smaller vs. a larger caster? What is the effect of a posterior caster?
2. What is the front rigging? How high above the floor should it be?
3. Why would an elevating legrest be used?
4. What are the six types of wheelchair cushions? What are the advantages and disadvantages of a Roho over a Jay cushion?
5. What is a grade aide?
6. What are four different control mechanisms for power WCs?

Answers:
1. Smaller casters have shorter turning radius but wobbles on uneven surfaces. A posterior caster decreases the turning radius, decreases stability, and increases maneuverability.
2. Front rigging refers to the footrest and legrest. It should have 2" of clearance above the floor.
3. An elevating legrest is used with decreasing dependent edema. It is used for BKA, knee extension contractures, and other joint abnormalities.
4. Contoured foam with gel insert (Jay), air-filled villous (Roho), gel-filled, coated contoured foam, foam, air-filled. A Roho provides the best pressure relief, but is high cost, less durable, and has poor seating stability.
5. A grade aide prevents the chair from rolling backwards and is helpful for patients with limited strength and endurance.
6. Joystick, head control (via headrest), chin control, sip and puff.

Wheels and tires

1. What is the most common type of wheelchair wheels? How do Mag wheels differ from spoke wheels?
2. What are the benefits of the posterior and anterior axle placement?
3. What are the advantages and disadvantages of solid rubber tires?
4. What are the advantages and disadvantages of pneumatic tires?
5. What is camber? How many degrees of camber maximizes lateral stability?
6. What are the advantages and disadvantages of increased camber?

Answers:
1. Mag wheels are most common, which are one piece and cast with metal alloy. They are maintenance free. Spoke wheels are lighter and easier to propel, but require more maintenance.
2. Posterior rear wheels give greater rolling resistance, more energy for propulsion, greater turning radius, and more stability (such as for loss of legs). Anterior rear wheels give less rolling resistance, less energy to propel, smaller turning radius, less stability, more maneuverability for possible "wheelies".
3. Solid rubber tires have a low rolling resistance on flat surfaces and there are no flat tires. However, they have less cushioning on bumpy surfaces and are heavy.
4. Pneumatic tires contain air and are lightweight for better ride on bumpy or carpeted surfaces but not as good on smooth surfaces.
5. Camber is the wheel angle with the vertical axis. 7 degrees maximizes lateral stability.
6. Higher camber makes the wheelchair easier to propel, increases stability, and tightens the turning radius. However, it increases the width of the chair, increases tire wear, and decreases seat height.

Armrests

1. How is the height of the armrest measured?
2. What are the advantages and disadvantages of fixed vs. removable armrests?
3. What are the advantages and disadvantages of full length vs. desk arm vs. adjustable height armrests?
4. What are the advantages and disadvantages of tubular vs. standard armrests?

Answers:
1. From buttocks to bottom of patient's bent elbow at 90 degrees plus one inch.
2. Fixed armrests are lighter but interfere with transfers.
3. Full length gives more arm support, but difficult to get under a table. Adjustabled height armrests are heavier than fixed.
4. Tubular armrests are more cosmetic, but can't be used with heavier individuals or for weight shifts.

Pressure relief backrests

1. What is a recliner backrest?
2. What are the advantages and disadvantages of using a recliner?
3. What is a tilt-in-space system? How much must it be able to tilt?
4. What are the advantages and disadvantages of tilt-in-space?

Answers:
1. A semirecliner can be adjusted to recline 30 degrees while a full recliner reclines to 90 degrees (and is 6 inches longer than the standard chair).
2. Advantages of the recliner is that it provides independent pressure relief, assists in orthostasis episodes, allows for PROM of hip and knees, mobilizes secretions, and aids catheterization. Disadvantages include resulting shear forces, increased spasticity, and increased turning radius.
3. The entire seat and back tilt as a single unit. It must be able to tilt at least 35-40 degrees to redistribute pressure.
4. Advantages are independent pressure relief, assistance in orthostasis, alleviates shear, no spasticity during position changes, maintains seating position during weight shifts, mobilizes secretions, tighter turning radius. Disadvantages include lack of ROM benefits, inferior pressure relief, difficulty maintaining items on lack, retrograde flow from leg bag, higher height, catheterization more difficult.

Wheelchair specifications

1. How does the vinyl sling seat differ from the solid seat?
2. How is the seat width determined? What problems result if this measurement is too narrow or too wide?
3. How is the seat depth measured? What problems result from a depth that is too shallow?
4. How is seat height measured? Why are some wheelchairs designed with seats closer to the floor?
5. How is the backrest measured?

Answers:
1. The vinyl sling seat is easy to fold, clean, and is lightweight. The solid seat is more firm and heavy but provides better postural control. It is also difficult to fold.
2. Seat width is 1 inch plus the distance of the widest point of the hips with clothing and braces. A narrow WC results in difficult transfers and skin breakdown. A wide WC compromises truncal support, leading to scoliosis, back pain, and difficulty with wheelchair propulsion.
3. Depth is measured from dorsal buttocks to popliteal fossa and subtract 2-3 inches. If too shallow, ischial pressure is increased and stability of the chair is decreased.
4. Height is measured from the bottom of the heel to the posterior thigh plus 2 inches. Hemiplegic WCs have seats closer to the floor so unaffected leg can propel the chair.
5. If the patient has good trunk control and can propel a WC, the backrest is measured from the bottom of the buttocks to the spine of the scapula minus 3 inches. If the patient has poor trunk control and can propel a WC, the backrest is measured from the bottom of the buttocks to the spine of the scapula minus 2 inches. If trunk control is poor and there is no upper extremity strength, a full measurement is taken going up the back with possible addition of a headrest.

Pump/surgical treatments of spasticity

1. What are the benefits of using a baclofen pump over oral baclofen?
2. What sort of patients are good candidates for a baclofen pump?
3. What are problems associated with a baclofen pump?
4. What is the SPLATT procedure? What procedure is it usually accompanied by?
5. What other orthopedic procedures treat spasticity?
6. How does a dorsal rhizotomy prevent spasticity?

Answers:
1. The pump is implanted in the subarachnoid space and delivers baclofen directly into the CSF, allowing high doses of baclofen without unwanted CNS side effects.
2. The pump is indicated for patients with diffuse, generalized spasticity with poor response to conservative treatment. Traditionally used in patients with spinal spasticity, SCI, MS, CP.
3. Tube dysfunction, pump failure, infection, dosage error, skin breakdown, spinal headache. Side effects of baclofen itself include drowsiness, headaches, dizziness, nausea, hypotension, weakness. Seizures, respiratory depression, and LOC can occur with overdose.
4. SPLATT (split anterior tibial tendon transfer) is used for treatment of equinovarus foot deformity (foot plantarflexed, inverted, and supinated). The tib ant muscle is split and the distal end is attached to the cuboid and third cuneiform bones, creating an eversion force. It is usually done in conjunction with tendo-Achilles lengthening.
5. Tendon transfers, tendon release, step-cut (Z-plasty) lengthening, tenotomy, myotomy.
6. Dorsal rhizotomy involves neurosurgical sectioning of selected dorsa; segmental roots to modulate afferent sensory input and reset muscle spindles so there is less spasticity.

Neurochemical reduction of spasticity

1. How are local anesthetics used in the treatment of spasticity?
2. How do chemical neurolytic agents work? How long are they effective for?
3. What are the side effects of phenol injections?
4. How does botulinum toxin work? What are its approved uses?
5. What is the usual dosing? How long is it effective for?
6. What are contraindications to receiving botulinum toxin?
7. What are common side effects of botulinum toxin?

Answers:
1. Local anesthetics like lidocaine or bupivacaine work by blocking the increase in permeability to Na ions normally associated with depolarization. It is used to determine the potential efficacy of a longer acting agent.
2. Chemical neurolytic agents like phenol or ethyl alcohol cause protein denaturation and axonal necrosis. They work from months to years.
3. Dysethesias (10-30%), muscle pain, muscle weakness, transient swelling, induration, DVT, sprains, skin slough, systemic reaction if injected intravascularly.
4. It produces denervation at the neuromuscular junction by blocking release of ACh. Approved uses include blepharospasm, strabismus, torticollis, and hemifacial spasm.
5. Dose is 25-200 units per muscle, maximum of 300-400 units per session, 3 months apart. Onset of action is usually 24-72 hrs after procedure but may take 7 days, peak is at 4-6 weeks, and it lasts 2-6 months.
6. Contraindications include sensitivity to botulinum, certain antibiotics (aminoglycosides, spectinomycin), myasthenia gravis, Lambert-Eaton syndrome, motor neuron disease, upper eyelid apraxia, pregnancy.
7. Side effects include weakness, hematoma, bruising, flu-like syndrome, dysphagia (from cervical injection), nerve trauma, local swelling, pain, local erythema, antibody formation.

Treatment of Spasticity

1. What measures can be taken to prevent spasticity?
2. What physical modalities and therapies are used to prevent spasticity?
3. How does baclofen work? What are the main side effects? What occurs if it is stopped suddenly?
4. How does diazepam work? What are the main side effects? What sort of patients should it be used with?
5. How does dantrolene work? What are the main side effects?
6. What are two central alpha-2 agonists used to treat spasticity? What are their main side effects?

Answers:
1. Daily stretching, avoidance of noxious stimuli (infection, pain, DVT, HO, pressure ulcers, urinary retention).
2. Heat, cold, stretching, splinting, serial casting, proper positioning, functional e-stim, vibration, relaxation techniques, motor re-education, biofeedback.
3. Baclofen is a GABA-B analog that binds to receptors in spinal cord, inhibiting the calcium influx. Side effect include sedation, weakness, GI symptoms, tremor, insomnia, and confusion. Withdrawal can cause seizures and hallucinations.
4. Diazepam acts on GABA-A receptors, facilitating post-synaptic effects of GABA, inhibiting muscle contraction. Side effects include sedation, so it is mainly useful in SCI patients rather than TBI.
5. Dantrolene acts peripherally on the striated muscle, blocking Ca release from SR, inhibiting muscle contraction. Side effects include hepatotoxicity (1%), sedation, weakness, fatigue, paresthesias, diarrhea, N/V.
6. Clonidine and tizanidine. Both cause hypotension, sedation, dry mouth. LFT monitoring is suggested with tizanidine.

Spasticity definition

1. What is the definition of muscle tone?
2. What is the difference between spasticity and rigidity?
3. What reflexes/tone are seen in a spastic limb?
4. What are the signs of upper motor neuron syndrome?
5. How is spasticty generally quantified?
6. What are complications or problems associated with spasticity?
7. What are benefits associated with spasticity?

Answers:
1. Muscle tone is the resistance of a muscle to passive stretch.
2. Spasticity is the velocity-dependent resistence to movement, caused by hyperexcitable stretch reflex. Rigidity is NON-velocity-dependent resistance to stretch.
3. Hypertonia, increased DTR and clonus, spread of reflex beyond the muscle stimulated.
4. Positive signs include spasticity, athetosis, primitive reflexes, rigidity, dystonia, decreased cutaneous reflexes, loss of precise autonomic control. Negative signs include weakness, paralysis, loss of dexterity, and fatigability.
5. The modified Ashworth scale is usually used: 0 is normal tone; 1 is increased tone with catch and release at end of ROM; 1+ is slight increase in tone through less than half of the ROM; 2 is marked increase in tone through more than half of ROM, but with full ROM; 3 is considerable increase in ROM with difficulty going through full range; 4 is affected part in rigid flexion or extension.
6. Interferes with function, painful, disfiguring, interferes with nursing care, contractures can form, predisposes to bone fractures, decub ulcers, interferes with hygiene, malunion of present fractures, joint subluxation/dislocation, increased HO, peripheral neuropathy.
7. Aids with ambulation, standing, and transfers, maintains muscle bulk, prevention of DVT, prevention of osteoporosis, decreased pressure ulcers over bony prominences, aids in diagnosis of noxious stimuli.

Concussion

1. What are the grades of concussion?
2. What are the Colorado Medical Society guidelines (endorsed by AAN) for return to play after a Grade 1 concussion?
3. Grade 2 concussion?
4. Grade 3 concussion?


Answers:
1. Grading system used is either the Cantu or Colorado systems. Colorado system: Grade I (mild) involves no LOC and confusion without amnesia. Grade II (moderate) involves no LOC and confusion with amnesia. Grade III (severe) involves LOC.
2. For a Grade 1 concussion, return to play after asymptomatic for 15 min or less. For multiple Grade 1 concussions, return to play after asymptomatic for 1 week.
3. For a Grade 2 concussion, return to play after asymptomatic for 1 week. For multiple Grade 2 concussions, return to play after asymptomatic for 2 weeks.
4. For a Grade 3 concussion, return to play after asymptomatic for 1 week if the LOC is only seconds. If the LOC is in minutes, return to play in 2 weeks. For multiple Grade 3 concussions, return to play 1 month or longer, based on decision of physician.

Mild TBI

1. What is the definition of mild TBI?
2. What are signs and symptoms of mild TBI?
3. What is the prognosis of mild TBI?
4. What is postconcussive syndrome?
5. What is the pharmacological treatment for postconcussive syndrome?

Answers:
1. Any physiologic disruption of brain function with at least 1/4 manifestations: any LOC less than 30 min, any loss of memory for events before/after injury, any alteration of mental status at time of injury lasting <24hrs,>12.
2. Headache (most common), dizziness, tinnitus, hearing loss, blurred vision, altered taste/smell, insomnia, sleep disturbances, fatigue, sensory impairments, attention/concentration deficits, slowed mental processing, memory impairment, lability, irritability, depression, anxiety.
3. Most have good recovery within 1-3 months.
4. Postconcussive syndrome is when symptoms persist and social/vocational difficulties occur that are out of proportion to severity of injury.
5. Antidepressants and psychostimulants.

Diabetes insipidus secondary to TBI

1. What is the cause of diabetes insipidus (DI)?
2. What sort of head fracture typically results in DI?
3. What are the symptoms of DI?
4. What are the findings in the urine and lab values?
5. What is the treatment of neurogenic DI?

Answers:
1. Deficiency of ADH (vasopressin).
2. Fracture near the sella turcica, resulting in tearing of the pituitary stalk. This disrupts ADH secretion from posterior pituitary, resulting in a neurogenic DI.
3. Polyuria, polydipsia. Dehydration is rare unless patient does not drink enough.
4. Urine concentration (<290mm/kg) is usually below serum concentration. Serum shows rising osmolality and rising Na concentration.
5. Desmopressin is an ADH analog that can be given intranasally or intramuscularly. Chlorpropamid potentiates effects of ADH on renal tubules and can be used in partial ADH deficiency.

Hyponatremia in TBI

1. What is SIADH? What are common causes of SIADH?
2. What are the symptoms of SIADH?
3. What is the treatment for mild, severe, and chronic SIADH?
4. What is the most common cause of hyponatremia in TBI?
5. What is the volume status of patients with SIADH? Cerebral salt wasting (CSW)?
6. What is the pathophysiology behind CSW? What are the symptoms?
7. How is CSW treated?

Answers:
1. Excessive ADH secretion from the neurohypophysis. Causes include head trauma, brain thrombotic or hemorrhagic events, CNS infections, lung disease, malignancy, and medications.
2. Mild SIADH may have no symptoms or anorexia, nausea/vomiting. Severe SIADH results in increased body weight, restlessness, irritability, confusion, coma, or convulsions. Peripheral edema is rare.
3. Fluid restriction (1L/day), monitor weight and Na levels. Hypertonic saline should only be used with severe symptoms and Na should not be increased by more than 10mEq/L in 24 hours. Chronic SIADH can be treated with demeclocycline, which inhibits ADH in the kidney.
4. Cerebral salt wasting.
5. SIADH is isovolemic. CSW is hypovolemic.
6. CSW occurs because of direct neural effect on renal tubular function, which causes Na to be lost in the urine. This results in hypovolemia, which triggers ADH secretion (which is appropriate in this case). Symptoms resemble that of dehydration.
7. Treat with fluid replacement and Na correction.

Urinary and cranial nerve dysfunction

1. What sort of incontinence is seen with TBI patients?
2. How is bladder dysfunction in TBI treated?
3. Which cranial nerves are most frequently affected by blunt head trauma?
4. How does damage to the olfactory nerve usually occur? What is the prognosis?
5. Why is the facial nerve especially vulnerable to being damaged?

Answers:
1. There is disinhibited detrusor reflex with small bladder volume that empties completely, resulting in small voids and normal PVRs.
2. Timed voids, and possibly anticholinergic meds to increase bladder capacity.
3. CN I (highest rate), VII, VIII more frequently. CN II, III, IV, and VI with intermediate frequency.
4. Displacement of the brain with tearing of the olfactory nerve filaments at the cribiform plate. It is associated with CSF rhinorrhea. Recovery occurs in >1/3 of cases, usually during the first 3 months.
5. Due to its long, tortuous course through the temporal bone.

Posttraumatic agitation

1. How long does posttraumatic agitation usually last?
2. What are environmental interventions that can be used to treat agitation?
3. What medications are used to treat agitation?

Answers:
1. 1-4 weeks, usually self-limited.
2. Reduce level of stimulation (quiet room, no noxious stimuli, limited visitors), protect patient and others (Craig (padded) bed, sitter, locked ward, mitts, helmet), reduce cognitive confusion (simple communication, familiar staff members), tolerate restlessness if possible (reduce physical restraints, floor bed, allow patient to pace or be verbally inappropriate).
3. Carbamazepine, TCAs, trazodone, beta-blockers, SSRIs, valproic acid, lithium, amantadine, buspirone, atypical antipsychotics. Avoid haloperidol, which decreases recovery of injured brain.

Treatment of posttraumatic seizures

1. When is phenytoin useful as prophylaxis against PTS?
2. What are the two drugs of choice for treatment of PTS? Why are these drugs thought to be superior?
3. How long should anticonvulsants be used?

Answers:
1. Only during the first week post-injury. Anticonvulsants are usually started after late seizures occur.
2. Carbamazepine (for partial seizures) and valproic acid (for generalized seizures) are preferred over phenytoin and phenobarbital due to less sedation and adverse cognitive effects.
3. After 1-2 years seizure-free interval.

Posttraumatic seizures

1. What are two kinds of posttraumatic seizures (PTS)? Which kind is more common?
2. How are PTS divided by their time post-injury? What kind has the worst prognosis? When do most PTS occur?
3. What are risk factures associated with late PTS?
4. How is PTS diagnosed?

Answers:
1. Generalized (grand mal and tonic clonic) and partial (simple if conscious, complex if not). Partial are more common.
2. Immediate PTS is within 24 hrs, early PTS is within first week, late PTS is after the first week. Early PTS is associated with the highest risk of late PTS. MOst PTS occur 1-3 months post injury.
3. Penetrating head injury, intracranial hematoma, early seizures, depressed skull fracture, prolonged coma, PTA. Less important risk factors are dural tearing, foreign bodies, aphasia, hemiplegia, age, alcohol abuse, tricyclic antidepressants.
4. Clinically, EEG, prolactin level (increased prolactin confirms seizure, but normal does not exclude seizure).

Venous thromboembolic disease

1. What is the most common first clinical sign of DVT?
2. What are factors associated with DVT?
3. What is Virchow's triad?
4. What are common prophylactic agents for DVT?
5. What are diagnostic tests for DVT?
6. How long is anticoagulation given in case of DVT?

Answers:
1. Sudden death (due to PE) in 70-80%.
2. Immobility, paresis, fracture, soft-tissue injury, age >40.
3. Venous stasis, vessel-wall damage, hypercoagulable state.
4. Low dose unfractionated heparin, LMWH, intermittent pneumatic compression, warfarin, IVC filter.
5. Doppler ultrasound, impedance plethysmography, I-fibrinogen scanning, contrast venography (gold standard).
6. 3-6 months.

More complications of TBI

1. How does tentorial (uncal) herniation occur?
2. What symptoms are produced from uncal herniation?
3. Why does post-TBI HTN occur?
4. What is the recommended treatment for post-TBI HTN?

Answers:
1. The medial part of one temporal lobe (uncus and parahippocampal gyrus) is displaced over the edge of the ipsilateral tentorium cerebelli as a result of increased supratentorial pressure from hematoma or brain tumor.
2. Stretching of CN III causes ipsilateral pupil dilation or third nerve palsy; ipsilateral hemiparesis from pressure on corticospinal tract; contralateral hemiparesis due to pressure on precentral motor cortex or internal capsule; late reduced consciousness.
3. Sympathetic hyperactivity, demonstrated by increased plasma and urine catecholamines.
4. Propranolol.

Heterotopic Ossification

1. What are the risk factors for heterotopic ossification (HO)? How long after injury is HO most likely to develop?
2. What are the symptoms of HO? What are the most common joints to be involved?
3. What are complications of HO?
4. What are tests used to diagnose HO?
5. What are methods and medications used to prevent HO?
6. How is HO treated?

Answers:
1. The risks are prolonged coma (>2 wks), immobility, limb spasticity, increased tone, long-bone fractures, pressure ulcers, edema. Most common 3-4 months post-injury.
2. Pain, decreased ROM, local swelling, erythema, warmth, muscle guarding, low-grade fever. The joints usually involved are hips (most common, elbows/shoulders, knees.
3. Decreased ROM, pain, bony ankylosis, peripheral nerve compression, vascular compression, lymphedema.
4. Serum alk phos, bone scan (very sensivitive, 2-4wks post-injury), plain films (used to confirm maturity of HO).
5. ROM, control of tone, NSAIDs, radiation (used in THA patients).
6. Diphosphonates, NSAIDs, ROM, surgery (after HO mature, at 12-18 months).

Guillain-Barre Syndrome (GBS)

1. What is the etiology of Guillain-Barre Syndrome (acute inflammatory demyelinating polyradiculopathy)?
2. What is the clinical presentation of GBS?
3. What is seen in the CSF?
4. What are the findings on EMG? What EMG findings are associated with a poorer prognosis?
5. What is the treatment?

Answers:
1. Post-viral autoimmune attack on myelin and Schwann cells that generally occurs 1-4 weeks post illness, vaccination, or surgery.
2. Ascending symmetry weakness and sensory abnormalities, areflexia, possible respiratory and autonomic failure, possible CN involvement (usually VII).
3. Increased protein, few mononuclear cells, called albumino-cytologic dissociation.
4. NCS shows abnormal SNAP, CMAP abnormal with increased temporal dispersion. F wave abnormal early in the disease. EMG is normal. Poor prognosis is associated with CMAP amp <20% normal, CV <40% normal, absent F waves, abnormal EMG.
5. Rehabilitation, plasmapheresis, IVIG, respiratory support Steroids have been found to be ineffective.

Elevated intracranial pressure (ICP) in TBI

1. What is a normal ICP? How is elevated ICP defined?
2. What is the relationship between ICP and cerebral perfusion pressure (CPP) and MAP?
3. What are indications for continuous monitoring of ICP?
4. What factors may increase ICP?
5. What are three methods used to monitor ICP?
6. What are common methods used to decrease ICP?

Answers:
1. Normal is 2-5mmHg. Elevated ICP is defined as >20mmHg for more than 5min. At >40mmHg, there is neurologic dysfunction and impairment. >60mmHg is fatal.
2. Increased ICP reduces CPP.
CPP = MAP - ICP.
3. Patient in coma (GCS <8) with CT findings of increased ICP; deep coma (GCS <6) without hematoma; severe chest and facial injuries with moderate/severe head injury (GCS<12); after evacuation of IC hemorrhage if pt in coma beforehand.
4. Fever, hyperglycemia, hyponatremia, seizures, turning head (especially to left side), loud noise, vigorous PT, chest PT, suctioning, hypertension.
5. Papilledema (develops in 12-24 hrs), CT scan, LP.
6. Elevate head of bed 30 degrees, hyperventilation (use with caution since this decreases brain PO2), osmotic agents (mannitol), furosemide, avoid HTN, barbiturates, surgical decompression. Hypothermia and steroids have not proven to be beneficial.

Posttraumatic hydrocephalus

1. What percentage of patients have ventricular dilation after TBI? What is it caused by?
2. What is the classic triad associated with hydrocephalus? What are common first manifestions in brain injury population?
3. What does CT scan show?
4. How is PTH treated?

Answers:
1. 40-72%, resulting from cerebral atrophy and focal infarction of brain tissue.
2. Incontinence, ataxia, dementia. With TBi, first manifestation may be HA, vomiting, confusion, drowsiness.
3. Periventricular lucency, lack of sulci, uniformity in ventricular dilation.
4. LP, shunt placement.

Head injury predictor scales

1. What is the Glasgow Outcome Scale (GOS)? How many categories are there?
2. What are the disadvantages of the GOS?
3. What is the Disability Rating Scale (DRS)?
4. What are the advantages of using the DRS over the GOS?
5. What is the Rancho Los Amigos Levels of cognitive function scale?

Answers:
1. The GOS is a 5 point scale rating outcome after brain injury: 1 is death, 2 is persistent VS, 3 is severe disability, 4 is moderate disability, 5 is good recovery. There's a correlation between GOS score at 6 and 12 months and outcome.
2. Categories are broad, scale not sensitive enough, not real indicator of functional abilities.
3. The DRS is a 30 point scale addressing 8 areas: eye opening, verbalization/communication, motor responsiveness, feeding, toileting, grooming, overall functioning independence, employability.
4. The DRS provides a quantitative index of disability that is more sensitive to clinical changes than GOS. It was developed specifically for disability.
5. This is an eight-level global scale focused on both cognition and behavior after TBI. It has a lower validity and reliability than the DRS.

Posttraumatic Amnesia

1. How is posttraumatic amnesia (PTA) defined?
2. What is the Galveston Orientation and Amnesia Test (GOAT)? How is it scored?
3. How does length of PTA relate to the severity of injury. How does PTA relate to prognosis?
4. What are other prognostic indicators in TBI?

Answers:
1. PTA is the interval of permanently lost memory following injury.
2. The GOAT is a standard technique for assessing PTA, involving orientation questions and memory. It is scored out of 100 pts and 75 is normal. A score of >75 on 2 days in a row marks the end of PTA.
3. 5-10 minutes PTA is mild, 1-24hrs is moderate, 1-7 days is severe, 1-4weeks is very severe, greater than 4 weeks is extremely severe. For moderate severity or less, a quick and full recovery should be expected. For a severe injury, residual deficits are expected.
4. Age (worse age<5>65), rate of early recovery, pupillary reaction to light, time since injury (most recovery within 6 months, use of phenytoin (=> adverse cognitive effects).

Glasgow Coma Scale (GCS)

1. What are three commonly used indicators of how severe a TBI is?
2. What are the three components to the GCS and how many points is each measured out of? Which is the best predictor of outcome?
3. What GCS score is the cutoff for coma? What range indicates severe injury? Moderate injury? Mild injury?
4. What is the Glasgow-Liege Scale and what does it measure?

Answers:
1. Best GCS within 24 hours of injury, length of coma, and duration of posttraumatic amnesia.
2. Motor (6), Verbal (5), Eyes (4), score 3 to 15. Motor is the best predictor of outcome.
3. GCS <8 is comatose. Score 3-8 is severe injury, 9 to 12 is moderate injury, 13-15 is mild injury.
4. This adds brainstem reflexes: the fronto-orbicular reflex (orbicularis oculi contraction with glabella percussion), oculovestibular reflex ("Doll's eyes" maneuver), pupillary light reflex, oculocardiac reflex (bradycardia caused by pressure on eyeball).

Posturing

1. What is the position of the arms and legs in decerebrate posturing? What are the characteristics of the face?
2. What sort of lesions cause decerebrate posturing?
3. What is the position of the limbs in decorticate posturing?
4. What sort of lesions cause decorticate posturing?

Answers:
1. Arms and legs are in extension, with ankles in plantarflexion and internal rotation of arms. There is also a clenched jaw.
2. Midbrain, cerebellar, or posterior fossa lesions.
3. Flexion and adduction of upper limbs and extension of lower limbs.
4. Higher level lesions: cerebral hemisphere/white matter, internal capsule, thalamic.

Disorders of consciousness: Minimally conscious state

1. What is the definition of minimally conscious state (MCS)?
2. What are behaviors that are seen in MCS? What are examples of reproducible behaviors?
3. What are signs that a patient is emerging from MCS?
4. What are therapeutic interventions that are used with all disorders of consciousness?
5. What are pharmacological interventions used with disorders of consciousness?

Answers:
1. Severely altered consciousness with minimal and inconsistent but definite reproducible behavioral evidence of self-awareness or environmental awareness.
2. Behaviors include visual fixation, smooth pursuit tracking, emotional or motor behaviors in response to specific stimuli. Reproducible behaviors include following simple commands, object manipulation, intelligent verbalization, yes/no responses (verbal or gestures).
3. Consistent following of commands, functional object use, reliable communication.
4. Management of bowel and bladder, nutrition, skin care, spasticity/contracture prevention, sensory stimulation, avoid overstimulation.
5. Eliminate unnecessary medications. Stimulation may be achieved via methylphenidate, dextroamphetamine, dopaminergic agonists, amantadine, bromocriptine, TCAs, SSRIs.

Disorders of consciousness

1. What two parts of the brain are responsible for consciousness?
2. What is a coma? How does it show up on EEG?
3. What is the mortality for comas lasting >6hrs? When does a coma generally evolve into a vegetative state (VS)? How can you tell this evolution has occurred?
4. What is a VS? When is it called a persistent VS or a permanent VS?
5. What are the characteristics of VS?
6. What is the neuropathology behind VS?

Answers:
1. The cerebral cortex and the ascending reticular activating system (cell bodies in the upper brain stem that project to cortex via thalamic and extrathalamic pathways).
2. A coma is an unconscious state in which the patient can't be aroused and there is no self or environmental awareness, no spontaneous purposeful movement, no localization of noxious stimuli, no language comprehension. EEG shows no sleep-wake cycles.
3. After >6hrs in coma, 50% patients die. In 2-4 weeks, comas evolve into vegetative states, which signals the return of brain stem arousal mechanisms in the face of thalamic, cortical and/or subcortical damage. Coma and VS are both characterized by absence of cerebral cortex activity. Transition to VS is signaled by eye opening, visual tracking, and spontaneous control of autonomic functions (respiration, CV, thermoregulation, neuroendocrine).
4. VS is loss of capacity to interact with environment despite preserved spontaneous or stimulus-induced arousal. It is called persistent VS >1 month after brain injury. It is called permanent VS either >3 months after nontraumatic brain injury or >12 months after TBI.
5. In VS, patient will open eyes, EEG shows sleep-wake cycles, no purposeful behavior, no signs of communication.
6. VS is related to diffuse cortical injury. Bilateral thalamic lesions are prominent findings.

TBI Recovery Mechanisms

1. What is brain plasticity? What influences it and what are the mechanisms by which it occurs?
2. How does neuronal regeneration differ from reorganization/unmasking?
3. What is diaschisis and how does it explain spontaneous return of brain function?
4. How does redundancy contribute to brain injury recovery?
5. How does vicariation contribute to brain injury recovery?

Answers:
1. Brain plasticity is the capability of the damaged brain to repair itself by morphologic and physiologic responses. It's influenced by the environment, stimulation, repetition of tasks, and motivation. It occurs by neuronal regeneration, collateral sprouting, and neural reorganization/unmasking.
2. Neuronal regeneration occurs when intact axons establish new synaptic connections via sprouting, occurring weeks to months post-injury. Functional reorganization/unmasking occurs when healthy neuronal structures are reassigned to a new function formerly done by the damaged area.
3. Diaschisis is when a lesion to one area of the brain produces altered function in another area of the brain that is connected to the damaged area by fiber tracts. Recovery of functions controlled by the remote site parallels recovery of the focal lesion.
4. Redundancy is when there are areas of uninjured brain that contributed to the function of the injured area, and after injury, take over that function.
5. Vicariation is when uninjured areas change their properties to take over the lost function.

Penetrating head injuries

1. What happens to a person whose brain is penetrated at lower levels of the brain stem?
2. What is the mortality rate from patients initially comatose from GSW to head? How does this compare to the mortality for a closed head injury?
3. How often do seizures occur in the early phase of a penetrating head injury?

Answers:
1. Death.
2. 80% mortality, 2x as high as for closed head injury.
3. 15-20%

Mechanisms of head injury details

1. What is a brain contusion and what sorts of deficits result?
2. Where in the brain is diffuse axonal injury seen and what is the mechanism of this injury?
3. What is the cause of brain swelling and when does it occur? How is it identified on CT?
4. What is the difference between brain swelling and brain edema?
5. What is the difference between vasogenic edema and cytogenic edema?

Answers:
1. It occurs on the undersurface of the frontal lobe and anterior temporal lobe, and can result from even a relatively low velocity impact. The deficits that result are focal, cognitive, and sensory-motor.
2. DAI is seen in the corpus collosum and other midline structures (parasagittal white matter, IV septum, walls of 3rd ventricle, and brain stem. It is responsible of a LOC during TBI. It results from acceleration-deceleration and rotations forces in high-velocity impact such as MVAs. There is damage to axonal transport causing increased Ca influx --> axonal swelling and detachment.
3. Brain swelling occurs within 24 of injury and is due to an increase in cerebral blood volume. On CT, it looks like a collapse of the ventricular system and loss of CSF cisterns around the midbrain.
4. Brain edema occurs later following injury than brain swelling. It is due to an increase in brain water content that leads to extravascular fluid.
5. Vasogenic edema is related to cerebral contusion and is due to outpouring of protein-rich fluid through vessels, resulting in extracellular edema. Cytogenic edema is related to hypoxic and ischemic brain damage and is due to failing of the cells' energy supply resulting in cell death and intracellular edema.

Mechanisms of head injury

1. What is a primary mechanism of injury?
2. What are some common primary mechanisms of injury?
3. What is a secondary mechanism of injury? When does it most commonly occur?
4. What are common causes of secondary injury?
5. How does increased release of excitatory neurotransmitters secondary to DAI result in secondary injury?

Answers:
1. Primary mechanism occurs at the moment of impact, as a direct result of the trauma.
2. Contusions and lacerations of brain surface, DAI, diffuse vascular injury, multiple petechial hemorrhages, cranial nerve injury.
3. Occurs after initial trauma, as a result of the injuring event. Usually first 12-24 hrs after injury, but may happen up to 5-10 days later if injury is severe.
4. Intracranial hemorrhage, brain edema, elevated ICP (resulting in decreased perfusion), hypoxic brain damage, intracranial infection, hydrocephalus, free radicals, excitotoxicity, hypotension, electrolyte imbalance, anemia, hypothermia, hyper/hypoglycemia, hypercarbia, hyponatremia, infection, carotid dissection, seizures, vasospasm.
5. This increases the activity of certain brain areas, resulting in increased overall metabolic demand in an already injured brain.

Epidemiology of TBI

1. What is the peak age for TBI?
2. What is the most common cause of TBI in adolescents and adults?
3. What is the most common cause of TBI resulting in death?
4. What is the mortality rate of TBI?
5. What is the most common cause of TBI in the elderly?
6. What are common causes of TBI in children?

Answers:
1. Bimodal distribution. Highest peak ages 15-18 to 25 years. Second peak ages 65-75 with higher mortality.
2. MVA.
3. Gunshot wounds, which have a mortality risk of 75-80%.
4. 14-30 per 100,000 per year.
5. Falls.
6. TBI is the leading cause of death in kids >1. From most common to least common, the causes are: Transportation, falls, sports, assault.

Peroneal neuropathy

1. What is the differential diagnosis of foot drop?
2. What is the etiology of peroneal nerve injury at the fibular head and what is the presentation? What are the EMG findings?
3. How is the deep peroneal nerve commonly injured? What is the presentation?
4. What muscles pass under the extensor retinaculum?
5. How is the superficial peroneal nerve commonly injured? What is the presentation?

Answers:
1. Diffuse polyneuropathy (diabetes), peroneal neuropathy, plexopathy, L4-L5 radiculopathy, tumor, CVA, AVM, SCI.
2. The peroneal nerve is injured at the fibular head by prolonged leg crossing, weight loss, poor positioning during surgery, poor cast application, prolonged squatting position (Strawberry picker's palsy), and metabolic disorders (diabetes). It presents with ankle DF weakness resulting in foot drop and steppage gait, with eversion weakness. EMG shows abnormal activity in peroneal-innervated muscles except for short head of biceps femoris.
3. The deep peroneal nerve is injured by compression from trauma or shoes as it passes under the extensor retinaculum (anterior tarsal tunnel syndrome). It presents with foot weakness (EDB) and atrophy with numbness in the first webspace. Pain is over dorsum of foot and relieved with motion. CMAP shows abnormal findings to EDB and EMG shows abnormal activity in the EDB.
4. Tibialis anterior, EHL, EDL.
5. Injury is by compression from trauma, ankle sprain, muscle herniation, or a lipoma. It presents with eversion weakness if injury is proximal and sensory loss.

Peroneal nerve anatomy

1. Where do the peroneal nerve fibers originate from?
2. What is the course of the peroneal nerve?
3. What muscles are innervated by the superficial peroneal nerve? What sensory branches does it give off?
4. What muscles are innervated by the deep peroneal nerve? What sensory branches does it give off?
5. What is the accessory peroneal nerve and how is it identified on NCS?

Answers:
1. L4-S2 roots, which becomes the sciatic nerve.
2. It branches from the sciatic nerve in the distal posterior thigh to form the common peroneal nerve. It then travels through the popliteal fossa, winds around the fibular head, then splits into the deep and superficial nerves. Prior to this, it gives off the lateral cutaneous nerve of the calf.
3. Peroneus longus, peroneus brevis. Sensory branches are the medial and lateral cutaneous nerve.
4. Tibialis anterior, EDL, EHL, peroneus tertius, EDB, FDI. Sensory branch is the dorsal distal cutaneous nerve.
5. The accessory peroneal nerve is an anomalous innervation. It branches from the superficial peroneal nerve, traveling behind the lateral malleolus to innervate all or some of the EDB. If there is a deep peroneal nerve injury, the EDB may be spared if there is an accessory peroneal nerve. NCS shows a CMAP with stimulation behind the lateral malleolus.

Sural nerve injury

1. Where does the sural nerve originate from?
2. What area does the sural nerve provide sensation to?
3. How is the sural nerve commonly injured?
4. How does sural neuropathy present?

Answers:
1. From branches of the tibial and common peroneal nerve. It passes from the proximal calf to the ankle posterior to the lateral malleolus.
2. The sural nerve provides sensation to the lateral calf and foot.
3. Compression from tight socks, Baker's cyst, laceration.
4. Abnormal sensation to the lateral calf and foot. There may be a positive Tinel's sign along the nerve.

Tibial nerve injury

1. What nerve roots does the tibial nerve come from?
2. What muscles are innervated by the tibial nerve? What sensory branches does it give off?
3. How is the tibial nerve injured in the tarsal tunnel? What structures pass through the tarsal tunnel?
4. What is the presentation of tarsal tunnel syndrome?
5. What are the NCS findings?

Answers:
1. L4, L5, S1, S2, which continues on as the sciatic nerve and then the tibial branch.
2. The tibial nerve innervates the plantaris, gastrocnemius, popliteus, and soleus. It then continues as the posterior tibial nerve to innervate the tibialis posterior, FDL, and FHL. It then runs underneath the flexor retinaculum and divides into the medial plantar nerve (adductor hallucis, FDB, FHB, lumbricals, sensory), lateral plantar nerve (lumbricals, ADM, quadratus plantae, sensory), and the calcaneal nerve (sensory).
3. The posterior tibial nerve is injured by compression under the flexor retinaculum. The tendons of the tibialis posterior, FDL, and FHL pass through the tarsal tunnel.
4. There may be symptoms of intrinsic foot weaknesss, perimalleolar pain, numbness, and paresthesias in the toes and soles, reproduced by ankle inversion. There may be a positive Tinel's at the ankle. Heel sensation may be spared due to calcaneal branch departing proximal to the tunnel.
5. SNAP is abnormal in plantar nerves but normal in calcaneal nerve. CMAP is abnormal in the medial and lateral plantar nerves.

Sciatic nerve injury

1. From what nerve roots does the sciatic nerve originate? What is the path of the nerve?
2. What muscles are innervated by the sciatic nerve?
3. Why is the sciatic nerve more susceptible to injury?
4. What sensory branches are given off directly by the sciatic nerve?
5. What are common causes of sciatic injury?
6. What are the symptoms and EMG findings in sciatic nerve injury?

Answers:
1. L4-S3. They become the posterior division of the lumbosacral plexus. It exits the pelvis through the greater sciatic foramen, between the greater trochanter and ischial tuberosity. It splits into the tibial and peroneal divisions in the mid-thigh.
2. The peroneal div innervates the short head of the biceps femoris. The tibial div innervates the long head of the biceps femoris, the semitendinosus, the semimembranosus, and the adductor magnus.
3. It is anchored at the fibular head.
4. The sural nerve.
5. Hip trauma, hip replacement, injection, hematoma, pelvic fx, penetrating wounds, pregnancy, piriformis syndrome (compression of sciatic nerve at pelvic outlet as it runs through piriformis).
6. Symptoms vary depending on which portion of the nerve is involved. NCS shows abnormal superficial peroneal and sural SNAPs, as well as tibial and peroneal CMAPs.