pbl2 - cns injuries

the latest pbl was about this dude getting shot in his back vertebrae, @L1+L2.

paralysis of foot->thighs.


so the issue was to find out about;
spinal cord anatomy
PTSD and other mental implications
effect to community

but i surreptitiously assigned everything to all my members, leaving myself with a free time to research what i want.

so i research about implications of SCI (Spinal Cord Injury) after the event.

Skin Breakdown: Skin breakdowns (also termed "decubitus ulcers" or "pressure sores" ) are a major complication associated with spinal cord injury. They occur as a result of excessive pressure, primarily over the bones of the buttock (particularly the ischial tuberosities and the trochanters at the hip). Following a spinal cord injury, there are not only changes in muscle tone and sensation, but shifts in the supply of blood to the skin and subcutaneous tissues. Additionally, there is a loss of the normal elastic nature of the tissues underlying the skin. Increased stiffness, vascular alterations and alterations in muscle tone combine to significantly reduce the skin's ability to withstand pressure. It is estimated that the closing "pressure" for skin breakdown is between 40 and 50 millimeters of mercury (about the same amount of pressure as placing a stamp onto an envelope). This complication is combated fairly aggressively through the use of pressure-relieving cushions that are either gel based or consist of a number of air bladders to reduce risk of the person "bottoming out". The cost associated with medical and/or surgical care of a single decubitus ulcer can run anywhere from $10,000 to $50,000 per admission. This does not take into consideration the loss of productivity if the individual is in the work place

Osteoporosis and Fractures: The majority of people with SCI develop osteoporosis. In people without SCI, the bones are kept strong through regular muscle activity or by bearing weight. When muscle activity is decreased or eliminated and the legs no longer bear the body's weight, they begin to lose calcium and phosphorus and become weak and brittle. It generally takes some time for osteoporosis to occur. In people who use standing frames or braces, osteoporosis is less of a problem. Generally, though, 2-t years following SCI some degree of bone loss will occur.

Using the legs to provide support in transferring is helpful in increasing the load on the bones, which may reduce or slow down the osteoporotic process. Standing using a standing frame or a standing table also helps prevent weakening of the bones and so does using braces for functional or parallel bar walking. Newer techniques, such as electrical stimulation of the leg muscles, may decrease osteoporosis as well.

Unfortunately, at the present time, there is no way to reverse osteoporosis once it has occurred. The main risk of osteoporosis is fracture. Once the bones become brittle, they fracture easily. An osteoporotic bone takes much longer to heal.

Pneumonia, Atelectasis, Aspiration: Patients with spinal cord injuries above the T4 level of injury are at risk to develop restriction in respiratory function, termed restrictive lung disease. This occurs five to 10 years following spinal cord injury and can be progressive in nature. The quadriplegic individual as part of a health care maintenance routine should have pulmonary function studies at yearly or every-other-year intervals between five and 10 years post injury. As the medical treatment of spinal cord-injured individuals continues to improve, respiratory complications of SCI are becoming more prominent. Adequate health maintenance and protection from this complication are appropriate and necessary as part of the long-term care of the spinal cord-injured individual.

Heterotopic Ossification: Heterotopic ossification is a condition not well understood that occurs in acute spinal cord injury and consists of the laying down of bone outside the normal skeleton, usually occurring at large joints such as the hips or knees. The primary problem with heterotopic ossification, or HO, is the risk for joint stiffening and fusion. Should the hip or knee become fused in a certain position, a surgical release is necessary to allow range of motion to occur. Unfortunately, it takes between 12 and 18 months for heterotopic bone to mature once it has developed. Activities that are used to prevent the development of HO include range of motion programs and other functional activities that move the joints within a functional range. Currently treatment is limited with the exception of preventing the joint fusion (termed ankylosis).

Spasticity: After spinal cord injury the nerve cells below the level of injury become disconnected from the brain. Following the period of spinal shock changes occur in the nerve cells that control muscle activity. Spasticity is an exaggeration of the normal reflexes that occur when the body is stimulated in certain ways. After spinal cord injury, when nerves below the injury become disconnected from those above, these responses become exaggerated.

Muscle spasms, or spasticity, can occur any time the body is stimulated below the injury. This is particularly noticeable when muscles are stretched or when there is something irritating the body below the injury. Pain, stretch, or other sensations from the body are transmitted to the spinal cord. Because of the disconnection, these sensations will cause the muscles to contract or spasm.

Almost anything can trigger spasticity. Some things, however, can make spasticity more of a problem. A bladder infection or kidney infection will often cause spasticity to increase a great deal. A skin breakdown will also increase spasms. In a person who does not perform regular range of motion exercises, muscles and joints become less flexible and almost any minor stimulation can cause severe spasticity.

Some spasticity may always be present. The best way to manage or reduce excessive spasms is to perform a daily range of motion exercise program. Avoiding situations such as bladder infections, skin breakdowns, or injuries to the feet and legs will also reduce spasticity. There are three primary medications used to treat spasticity, baclofen, Valium, and Dantrium. All have some side effects and do not completely eliminate spasticity.

There are some benefits to spasticity. It can serve as a warning mechanism to identify pain or problems in areas where there is no sensation. Many people know when a urinary tract infection is coming on by the increase in muscle spasms. Spasticity also helps to maintain muscle size and bone strength. It does not replace walking, but it does help to some degree in preventing osteoporosis. Spasticity helps maintain circulation in the legs and can be used to improve certain functional activities such as performing transfers or walking with braces. For these reasons, treatment is usually started only when spasticity interferes with sleep or limits an individual's functional capacity

Deep vein thrombosis: (DVT) or pulmonary embolism is a potentially severe complication of spinal cord injury. As mentioned above, there are changes in the normal neurologic control of the blood vessels that can result in stasis or "sludging". Deep vein thrombosis in the lower leg is almost universal during the early phases of recovery and rehabilitation. Thromboses in the thigh, however, are a great concern, as they are at risk for becoming dislodged and passing through the vascular tree to the lungs. A major obstruction of the arteries leading to the lung can potentially be fatal. Therapeutic measures to reduce or eliminate the risk for deep vein thrombosis include Ace wrapping of the legs and the use of pneumatic compression stockings. Medications administered subcutaneously, such as heparin, are useful in reducing blood viscosity and improving flow. In the event that a thrombosis develops, treatment is begun with intravenous heparin. Once adequate anticoagulation is provided, the patient is switched to or medication, called Coumadin

cont.

spinal shock

pinal shock was first defined by Whytt in 1750 as a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) -- most often a complete transection. Reflexes in the spinal cord caudal to the SCI are depressed (hyporeflexia) or absent (areflexia), while those rostral to the SCI remain unaffected. Note that the 'shock' in spinal shock does not refer to circulatory collapse.
Contents [hide]
1 Phases of Spinal Shock
1.1 Explanation of Phases
2 Autonomic Effects
3 References
[edit]Phases of Spinal Shock

Phase Time Physical exam finding Underlying physiological event
1 0-1d Areflexia/Hyporeflexia Loss of descending facilitation
2 1-3d Initial reflex return Denervation supersensitivity
3 1-4w Hyperreflexia (initial) Axon-supported synapse growth
4 1-12m Hyperreflexia, Spasticity Soma-supported synapse growth
[edit]Explanation of Phases
Ditunno et al. proposed a four-phase model for spinal shock in 2004.
Phase 1 is characterized by a complete loss -- or weakening -- of all reflexes below the SCI. This phase lasts for a day. The neurons involved in various reflex arcs normally receive a basal level of excitatory stimulation from the brain. After an SCI, these cells lose this input, and the neurons involved become hyperpolarized and therefore less responsive to stimuli.
Phase 2 occurs over the next two days, and is characterized by the return of some, but not all, reflexes below the SCI. The first reflexes to reappear are polysynaptic in nature, such as the bulbocavernosus reflex. Monosynaptic reflexes, such as the deep tendon reflexes, are not restored until Phase 3. Note that restoration of reflexes is not rostral to caudal as previously (and commonly) believed, but instead proceeds from polysynaptic to monosynaptic. The reason reflexes return is the hypersensitivity of reflex muscles following denervation -- more receptors for neurotransmitters are expressed and are therefore easier to stimulate.
Phases 3 and 4 are characterized by hyperreflexia, or abnormally strong reflexes usually produced with minimal stimulation. Interneurons and lower motor neurons below the SCI begin sprouting, attempting to re-establish synapses. The first synapses to form are from shorter axons, usually from interneurons; this is Phase 3. Phase 4, on the other hand, is soma-mediated, and as it takes longer for axonal transport to push growth factors and proteins from soma to the end of the axon, it takes longer.
[edit]Autonomic Effects

In spinal cord injuries above T6, autonomic dysreflexia may occur, from the loss of autonomic innervation from the brain. Sacral parasympathetics (S2-S4) are lost, as are many sympathetic levels, depending on the level of the SCI. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrythmias -- which resolve in 3-6 weeks. Autonomic dysreflexia is permanent, and occurs from Phase 4 onwards. It is characterized by unchecked sympathetic stimulation below the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of bladder/bowel control, sweating, headaches, and other sympathetic effects.