Hemiplegia - One side of the body involved. The opposite side of the brain probably lost flow to the middle cerebral artery by any of several means. Hemorrhage can also do this. Typical of hemiplegia is more dense involvement of the arm than of the leg as the hand and arm representation on the brain surface is in an area with less cross flow from other vessels. Children with four limbs involved with the uppers more than the lowers in a pattern of elbow & wrist flexion and leg extension are often called bilateral hemiplegia (rather than quadriplegia) to emphasize the pattern of involvement rather than just a limb count (duh). In effect, both middle cerebral arteries were compromised or bilateral hemorrhages occurred. Sudden low blood flow might involve the middle cerebral territory most as there is least cross flow from other vessels (at full term, this is not so earlier in development). It would seem that the brain surface, anticipating birth shearing of the skull drops cross connecting vessels that were feeding the brain surface.

Quadriplegia - in the context of this list this term is OK, but not best - It implies a very generalized event, such as anoxia. There can be good flow with poor oxygenation such as is caused by placental disconnection. The child's heart pumps but the blood gets no oxygen. CO₂ also builds, as does acidosis. Damage is to those areas most sensitive to oxygen deficit and to acidosis. The base of brain is particularly involved and is most eleptogenic. Cerebellum and other areas are also involved. Generally involvement manifests very severely in the legs with a different pattern of arm paralysis than seen in stroke. Actually a better term is Total Body, as such children seldom have head and neck spared.

Diplegia - Spastic Diplegia is nearly ¹/₃ of cases of CP and primarily related to prematurity. The brain shows a change called peri-ventricular leukomalacia (PVL). This translates as clear whitish soft spots (necrosis) scattered around the ventricles. Why there? In preemies, the brain surface just on the shore line of the fluid filled ventricles has least blood vessel access as no vessels cross the ventricles. A low-flow event will manifest here. The worst area is near where tracts representing the lower legs are passing by. The tracts from the body form a boomerang shape in cross section horizontally. That shape carries certain nerve fibers away from danger.

As the flow insult worsens, the damage spread will bring in more representation of the body and  even a bit from  hands. Nestled in the hollow of the boomerang, however are other structures which are associative. As hands get more involved (the scope of injury larger) the chances that these associative areas will also suffer, increases. In this group there is an association between more hand involvement and more learning difficulties.

The spasticity in spastic diplegia tends to be the purest, if free of the mid-brain kinds of tone abnormalities. The range of motion loss is worse with rapid testing than with slow movement testing, as the circuits most involved are those that interact with the velocity detection mechanism.

The more severe involvement has considerable hand and arm involvement, perhaps only on one side. However, such four limb involvement is quite unlike that seen in total body involvement as the neurologic injury is different.

Triplegia - Hard to know what this term means. Most of the time it is spastic diplegia + hemiplegia. That is, periventricular leukomalacia (diplegia) plus a stroke.

Dystonia - Certain mid brain structures when faulted will leave a condition not too unlike Parkinson's disease, as it is the same anatomy, essentially. Stiffness of initiation of movement and movement is the feature. That stiffness feels uniform and unrelated to speed of testing. It is very apt to change quality and form when sensation picks up change (earache, tooth ache, bladder infection, finger injury etc.).

Rigidity - is another kind of stiffness wherein the stiffness of one joint is related to the posture of the next joint. Thus an ankle very rigidly pointed downward at an extreme and feeling like stone, suddenly points upward when the knee is flexed. Likewise the hip responds to knee position or the reverse. We see thrust or withdraw patterns to these associations which stem from the mid-brain primitive circuits intact without higher level inhibition.

Athetosis - is an oscillating rhythmic movement of the limbs often associated with extremes of facial movements, though not always. A very specific area in the brain does this when injured. It can be injured by high bilirubin (jaundice) levels. Today that is rare, although we have seen it increase in the wake of drive by birthing, as the detection skills at home my be wanting. It was a complication of parental Rh Factor incompatibility before the newer preventative measures were made standard procedure. Today, athetoid cerebral palsy probably occurs in the full term infant who undergoes a brief but profound anoxic event, implicating oxygen sensitivity. This makes sense as similar disorder is seen in carbon monoxide poisoning. Interestingly, the movement disorder of CO poisoning shows up months after everybody has celebrated the good fortune of surviving. Babies with athetoid cerebral palsy often do not manifest the disorder until one to two years. They may be described as a bit floppy at birth, however. The thinking is that the damage may be to supportive cells that are woven like lace through the brain. Absent these cells, the neuro elements then wither, late.



Neurons must divide to increase their number then sprout long branching filaments which must migrate among billions of other neurons to form associative connections. Substances that affect the minds of adults do so by neurochemistry. Alcohol affects neuro chemistry. Anything that affects neurochemistry might also affect the stepwise processes of brain formation: division, migration, connection and also myelination (a special coating to make conduction faster). So, alcohol ruins baby brains. Cocaine does it in most subtle but scary ways (impulsive children blind of consequences). Low thyroid function, uncorrected, guarantees profoundly low IQ.
When you list the really bad causes of developmental brain conditions we find many can be prevented.

Terminology & Reality: It is difficult to discuss this subject without first having yet another snit about customary medical  terminology. The official categorization of neurologic injury which is deeply ingrained into medical "codes" (computer classifications for insurers) is based on the ability to count to four. So, if a person with neurologic injury has only one limb impaired that is monoplegia; two limbs impaired, diplegia; three limbs is tri plegia. Four is quadriplegia. Four limbs with body and head is total body. But what USEFUL information does that convey? This classification is worse than useless. It is annoying. Aside from the fact that the limbs are not the site of injury but just taking orders as sent, the terminology homogenizes many causes. Imagine if we only had the word tree for that collection of upright plants. So much for ash, elm, oak, maple, catalpa, evergreen, spruce, balsam, birch, tulip, aspen, fir, cypress, juniper, larch, tamarack, pine, cedar, beech, chestnut, eucalyptus, hickory, walnut, sycamore, ailanthus, magnolia, olive, fig, ficus, plane, palm, willow, locust, sequoia, redwood, poplar, acacia, cottonwood, beech, box elder, apple, crabapple, redbud, mulberry, cherry, peach, plum, pear, prune, banyan, baobab, bamboo, abba, calabra, betel, mahogany, ebony, bo, ironwood, dogwood, ginko, bottle, or bonsai, burned, worm ridden, moss covered or whatever. Mono, di, tri, quad. That's it? Working clinicians have morphed this insisted (encysted?) terminology into a more useful - though confusing - shorthand code which, hopefully, goes unnoticed by administrators, in order that it serve a more useful purpose - treatment. For treatment we need descriptions based on the presumptive neurologic types and shapes of brain injury as it affects capability. From that, we can infer approximate resultant functional consequences. Diplegia: So, diplegia ("two limbs weak") has come to mean that which results from tiny speckled white infarcts (or small hemorrhages) scattered just outside the periphery of the ventricles of the brain ( whether two limbs are involved or not ). In microscopist lingo that description becomes periventricular leukomalacia (PVL). Peri= around, ventricular=relative to ventricles (fluid cysterns in the brain), leuko = white or clear colored, malacia= oooy gooey or mush, or pathologically "soft". The premature brain has a network of extra blood vessels that deliver blood to the brain surface or cortex. That is protective of the cortex when flow pressure drops for any reason. The lease served area for extra flow is adjacent the ventricles as that is a fluid region devoid of solid structures. Adjacent the ventricles (periventricular) is bay side property. When the winds of trouble blow in the preemie, the bay side property gets hit most. When PVL speckled damage is confined to a small region, manifestation of malfunction may well be in the legs only. Perhaps, just the ankles. Maybe just a trace of ankle reflex sensitivity not even noticed clinically at all. Typical PVL can be one sided in which case the diplegia is really only one leg ( hemi-diplegia ). As the scope of these small PVL injuries scatters further out in a larger radius into  the periventricular brain suburbs, hands and arms may also be involved somewhat. Even so, we still don't call it quadriplegia.  The peculiar pattern and quality of muscular usage is what is important. PVL or "diplegia" conveys that. So diplegia - forget that di means two - may well have four limbs involved. The dominant manifestation is legs AND in a certain way. There is a unique quality to the way diplegia function is impaired. Lately, even parents are referring to their children as having PVL. Good . That tosses out the old misleading nomenclature. I like that. PVL is a very common neurologic complication in preemies. One third of all CP is prematurity related and thus have the PVL type of neurologic based involvement. The classic look of diplegia (PVL) is inward rotation crouch. The typical functional limitation is via speed related recruitment of unasked for muscular activation (speed related recruitment of additional muscle activity is called spasticity. Anything else which is called spasticity is called that WRONGLY!!!!) It is an important distinction. Kids with high levels of spasticity may have their control mechanisms intact, but, overloaded with extraneous stuff. Sensory mechanisms are usually working. Remember that prematurity is itself a complication of something else. There can be incompetent cervix or twin / triplet  issues. But  prematurity may brought on by genetic problems within the child's genome causing late spontaneous abortion. The earlier the prematurity, the more likely an underlying embryologic or fetal cause is also present. Nit picking? No. Don't get blinded by statistics. Statistics do not cause. They report. You can simply report that last year 0.001% of the population got run down by trucks (I made that number up) - and/or - you can advise that folks don't stand in highways. Percent relatedness of CP to prematurity is a batting average. The idea is to avoid being a statistic. Look to causation. Maybe the first truck just brushed you, but a bigger wider one is bearing down? Turns out that of the 0.001% who are hit by trucks, 80% are run over by six more following cars. Ouch. That's the point. When brushed by a truck, don't stand there giving the trucker the finger.    Move!   Fortunately, outside the ventricles the brain has a superhighway of up and down going motor and sensory pathways made mostly of cell projections (and not the cell bodies themselves. Conduits. The motor lanes that involve the legs are most central. As you go from the feet upward, neurologic input paths layer on top and thus are further from center. Geometry figures in diplegia. The range of severity in diplegia correlates with the concentric layering on of motor pathways as you travel up the spinal cord and to the brain past the ventricles. Closest to the ventricles are the projections from the foot and ankle. Furthest away are those from the neck. So, just foot involvement means a small radius of damage. Hand or neck involvement implies a large radius of damage which may well overlap other kinds structures. Other kinds, closest are the basal ganglia (wherein damage can generate rigidness and / or dystonic types of inappropriate muscular signals (described below). Quadriplegia & Ataxia: Quadriplegia, on the other hand, is what is seen after diffuse anoxic (no O2) brain injury. The pattern of brain involvement reflects damage where ever the brain's metabolic rate most demands oxygen and also where tissues are most easily damaged by concomitant CO2 build up (which makes acid). The really important stuff, the basic richly cellular deeper  brain base regions are highly metabolic and thus sensitive to oxygen deprivation and CO2 excess. This is true in adults as well as children. Carbon monoxide poisoning, for example, disables hemoglobin such that oxygen can't get delivered by the red blood cells. Those basal brain structures which use much oxygen get damaged first. These cells are NOT only neurons, but also include cell types which support brain structure and which nurture neurons. Interestingly, the effects of damage to these cells may not be apparent initially. Damage to supportive cells may take quite a while to manifest as secondarliy affected neurons become more disabled by the lack of nurture from damaged  supportive cells. Survivors of carbon monoxide poisoning ("Hero Girl Scout Pulls Unconscious Man From Running Car In Garage. Man is fine.") may slowly reveal the initially unseen damage over months or even years. ("Man Exposed to Fumes, Claims Walking Lost. Insurer Cries Fake- citing newsreels of him intact.") The typical basal ganglia insult will manifest over about two years. Children with ataxia, or athetosis often don't get diagnosed for that length of time. It doesn't mean that the symptoms were missed. It may well mean that the neuron manifestations evolved over time. Below the ventricles, spreading large blotches or lakes of injury may be found positioned along key brain centers called ganglia. Ganglia are centers rich in cell bodies, rather than just the long filamentous extensions (called dendrites). These cell bodies do the brunt of metabolic work which they pass along to the long networking extensions. Cerebellum related ganglia and base of brain ganglia, when disordered, attack balance and mid line function - trunk, speech, breathing, coordinated eye symmetry etc. It may also involve specific portions which create a high incidence of severe and hard to control seizure activity. Quadriplegias often have gross thrusting postures. Certain ganglia, when injured, cause some joints to posture oddly in reaction to perceived postures of neighboring  joints. Thus, a flexion of the wrist may initiate an extension of the nearest knuckles which then causes the next in line knuckles to flex while the elbow goes into a responding contortion of its own. That cascade of alternating postures of sequential joints is called dystonia. Some are symmetric and some are asymmetric. Rigidity is when injury to deep ganglia cause a very high sustained tone which manifests on both sides of joints - making them feel rigid - or frozen. Hemiplegia: Blockage Hemiplegia is most commonly from those injuries that follow loss of blood flow along the middle cerebral artery. This is key. Diplegia is speckles of injury adjacent the ventricles. Quadriplegia, damage to oxygen sensitive tissues. Hemiplegia maps along delivery lanes - blood vessels. We are discussing arterial delivery - the paths along which blood flows. The understanding of involvement reflects the distribution of specific blood vessels. Regions of brain served by the middle cerebral artery but which also have alternate blood flow from nearby vessels will be spared or transiently involved then recover. The zone of brain supplied by the middle cerebral artery minus those portions which also get blood supply from elsewhere is the distribution area of brain injury. That gives a characteristic pattern of involvement. An arterial blockage may produce a very small deficit if collateral (extra) arteries are abundant and well connected. Preemies have many extra temporary arteries covering the brain surface and thus seldom show typical hemiplegia patterns (at least those caused by single artery blockage). In anticipation of the shearing caused by the floating skull plates in the birth process, these extra vessels from the outer surface are removed late in pregnancy. Bleeding But hemiplegias may also result from a right sided or a left sided intracranial hemorrhage (bleeding). In this case,  damage is less road-like (following the artery) and more lake-like (under the pool of bleeding). Occasionally the bleeding, by sheer volume, can displace the brain and cause secondary injuries well away from the prime bleeding area. These secondary injuries caused by herniation from pressure or shifting also need to be addressed as additional injuries on top of the hemiplegia. There are only three main arteries. The middle one is the most at risk, hence the typical pattern of damage. Direct Trauma Hemiplegia may also result from direct trauma to the side of the head. Because of the infinite ways one side of the brain can be wounded, there are many many subtypes within this designation. Anywhere a trauma may land, a different kind of functional loss can occur. An exactly similar wound in one spot can cause loss of use of one arm. Moved slightly it could instead damage speech. Moved another way, a blind spot may occur or perhaps a specific memory disorder... maybe behavioral inhibitions get lost. Like piano keys, same press in different places give differing notes.   Common Patterns The most common postural pattern, that caused by arterial blockage, has the elbow and wrist flexed and the upper extremity more deficient of hand and arm function than is the leg of walking function. Sensation and self recognition of the part is often impaired as much or even more than movement per se. Sensory or positional recognition is a serious component of these hemiplegias. We use this designation regardless of how many limbs are involved (mono, di, tri, quad). We might see half of a hemiplegia. (Who says the entire length of the artery has to be involved?) The full pattern - if bilateral - is called double hemiplegia rather than quadriplegia because it better describes the characteristic distribution of posture and sensory deficits seen in the arms and legs than does "quadriplegia" - something of totally differing cause and behavior. Left brain damage may well also include those brain regions that process what we call language as words - that is - matching words to thought and matching sounds to selected words and then actually speaking the words. If the damage is on the right side then speech facility may be normal but it may be lacking in projection of and void of nuance intonation. Receptively, sensory side, words may be understood only by dictionary meaning missing the meaning gleaned from intonation and context - right brain talents. Something very vexing in hemiplegia from head trauma - especially and peculiarly from head trauma - is disease denial. It runs this way: If I use a cane that means I have weakness. Therefore, if I refuse the cane - I won't have that weakness. This ill-logic is maddening to family wearing themselves out trying to go through logic lists in the hopes of getting correct conclusions and therefore cooperation from the patient. Sensory disorder, in hemiplegia, often goes unnoticed even though it is what limits function. In fact, sensory abnormalities what limit use regardless of posture or ability to perform requested movements. Most importantly - from a reconstructive point of view - no matter how well movement is established and posture improved, function will not follow if sensory deficits do not allow a perception of change. Stated in another way: There is far more to be gained by sensory recovery than by motor recovery. Recovery has two main forms. 1: In acute trauma, larger areas of brain are "dazed" than destroyed. As these areas reacquire function we see "recovery". The most central area of damage may well persist but key functions might nevertheless return. 2: In babies, whose brains are not complete at birth, function might become reassigned to other parts of the brain well away from the damage. These brain areas are not at all those we would normally associate with the function which returns. The designations found in anatomy texts indicating normal adult regions of function do not, therefore, tell us what we really want to know. Will this loss recover? There is recent genetic evidence that a major key to outcome is in the genetics of neurologic healing which is, in essence, the genetic ability to reassign function from injured areas to intact areas of brain - even to the opposite side. Also in this is the reason that speech is so often intact in children whose brain injuries would be expected to eliminate speech. Certain genes have been noted to correlate with high levels of injury reversal. Others with poor recovery. The ultimate outcome may be more related to degree of recovery than to the initial scope of injury. In fact a very nit picking and fastidious study of new born babies found 7 times the number of subtle neurologic findings than any of our clinical data (from toddlers) had suggested. The conclusion is that our data of incidence of clinical CP reflects a lower number of injuries - by far - than actually initially occur. MOST heal. MOST. The span of time was considered to be about seven years. This data is in flux. New information seems to support these figures as a generality. So, late brain injury, injury after function has been assigned and hard wired - is different from early brain injury - before the function is up and running. The plastic infant brain can decide - so to speak - to place the needed function in an intact though odd location. Injury to the speech center location is different if the injury follows attainment of speech than if before speech is up and running and the center for that function uncommitted. Hemiplegia Subtypes Let's look at the big three subtypes of hemiplegia before considering the sensory aspects. There is gross mass action type, locked knee type, and free knee type. Gross mass action type can be likened to the entire body on one side - from shoulder to toes - being as if of wood, solid. There is very little actual hip motion if you look closely. Most are fooled and miss that fact. In, say, a left dense hemiplegia, what happens in walking is that when you think the left hip is flexing you didn't notice that the torso leans back as much as the thigh "flexes" forward. So, in actuality, left hip flexion is occurring through the RIGHT hip. The intact side develops a really complex mode of movement. The right side is doing everything. It lifts the left hemi-body off the floor and tilts the entire left side so as to advance the foot forward and then sets the stiff left side down. Once firmly set down the right side pole vaults, using the rigid left side as the pole. The left hip joint does nothing. Attacking the left hip flexibility will accomplish nothing. In fact, the rigidity of the left hip and knee help, as the right side could not depend on what the left side might do if it varied unexpectedly without sharing (proprioception) how it was varying. In essence it is a peg leg on the left with the entire left side of the body (shoulder to toe) being the peg. Gait is totally right sided and proprioception is totally right sided. A dense right hemiplegia is the flip of the above. Free Hip Type. The free hip type means free hip and only the hip is free. That is, the right knee behaves stiffly. The stiff knee supports weight. As long as hip mobility has proprioception (position sense) then the motion may be useful. If not, the motion may translate into instability. The good side needs to know where the opposite foot will be - either by feel or by reliability (as with a peg leg). In the free hip but stiff knee cases the lure is toward better more energy efficient walking. Despite all the many determinants of gait that have been discussed, in this group the only factor that works or not is flexion of the involved side knee BEFORE the leg swings. Unfortunately, gait lingo defines swing phase as when the toe moves foward. More unfortunately, that was the worst of all possible definitions. An amputee with no knee at all can have a fairly decent walking pattern if the prosthetic knee allows an early swing of the thigh without acting like a brake. Forget established gait analysis lingo - it is hopelessly wrongly outdated from the newer understanding. What swings in walking is the THIGH. Thigh swing is the event to watch (In old lingo that was called preswing). Watch? Why? If it is stiff, won't making it flexible just make it unreliable? Maybe. There are two kinds of stiff knee hemiplegia patients. One is a truly neurologically stiff knee. The other is not stiff at all, but made to appear stiff because of the foot ankle mechanism. Some are both. The last first. If the foot is stiffly in a down pointing posture, then when weight lands on the foot the toe hits first and then the heel. The stiff ankle link will thrust the tibia backward and thus lock the knee. The backward thrust tibia with weight on it will lock like a baby carriage lock and prevent knee flexion. That way swing is blocked by the downward pointing foot. This is called "ground reaction". Ground reaction is not seen only in hemiplegia. It is, however, a particularly prominent source of difficulty in walking in hemplegia. If you cast or AFO the ankle into dorsiflexion leaving a flexible metatarsal (ball of foot) roll over (flexible or absent toe plate), then the ground reaction ought to disappear and swing phase knee flexion resume. If that is what happens then attention to the ankle mechanics will tremendously improve walking. Some of the stiff knee walkers are stiff in the knee because the quadriceps group of (4) muscles fires just at or before swing phase. In other words, the quadriceps muscle thinks it is one of the hip flexor muscles and is firing along with the hip flexor group. It is the hip flexors which initiate swing phase. Look closely at the quadriceps and notice that one of the four parts of that muscle group does not attach to the femur (thigh) bone but rather extends up to the pelvis and can be recruited as a supplemental hip flexor. We use it that way when we need additional power. However, if that circuitry runs amok, then the quadriceps muscle fires with the hip flexors in walking (ought not) and may recruit by reflex the rest of the muscle group. The portion of the quadriceps which extends above to the pelvis is called the Rectus Femoris. If the rectus femoris is simply reacting to stretch when the thigh is extended, then releasing the upper end from the pelvis will solve the problem. If, however, the rectus femoris is acting solely by mass action with the flexors then detaching it distally and even reattaching it on the flexion side of the knee will reduce some of that knee locking. Some. Not all, as the recruited portions may still trigger but less so. This transfer was worked out by Dr. Perry at Ranchos Los Amigos where many adult stroke patients are treated. Some of the childhood hemiplegias have similar reactivity and may be candidates for that transfer. There is a danger. When hamstrings are firing very strongly, the quadriceps may have to counter fire to allow weight bearing. That COMPENSATORY over firing can be misinterpreted as mass action quadriceps activity. There are many kids who are getting routine transfers of the rectus femoris at the time they are having hamstring lengthening. In our experience, this reflects that more hamstring is being blamed for overactivity than ought to be. The high velocity components trigger the slower components (which are far stronger). We feel that if you attack the high velocity portions, then the rest quiets down and the apparent mass action goes away. Why? Not all mass reaction is from the brain. We were able to mimic this phenomenon in NORMAL volunteers by using elastics that required strong output to overcome (see elastics). Mass action is a normal process in motion under high tension. So? The way to distinguish is to play with motion to see if speed induces the prefiring (premature muscle action) or rather caused by reaction to high resistance regardless of speed. Big difference. There is a fourth type, named in error, which is really an extended diplegia (PVL) spared on one side. You can also add other mislabeled types as well given single side sparing. But the reverse is also true. We  see some true hemiplegia types (from any of the three main sorts listed above) added on to other kinds - say diplegia plus stroke.   Sensory Side Issues Sensory. Just what is sensory? Well the obvious is sense of touch - for sure. But a whole bunch of other stuff is sensory as well. With your eyes closed, where is your left great toe? Point to it. That obvious knowing of where that and the other parts are located is called proprioception as was the guidance in pointing. Pull an elastic and hold it stretched. How much tension is this pull? How did you know when to stop? Dip a spoon in water. Then feel it. How warm is that? Feel the electric clock. Is that thing vibrating? Have somebody spell a word or draw a shape on your palm with your eyes closed. What was written? Was it a circle or a heart shape? Can you draw a happy face in the air with your eyes shut? Your are sledding down a hill with eyes shut. Can you tell when the hill levels out? Can you tell about how fast you went? Can you tell when to put your feet down because you are about ready to hit those trees again? Somebody called you. How far away? From where? Oooo. I know that smell. That light in the distance seems to be getting nearer. This ground feels soft. There is a whole bunch more. Getting under a pop up fly ball in order to catch it requires a complex calculation of trajectory taken from the perceived ascent  (downward is way too late, unless you are a really fast runner). To sit on that chair over there, do you first turn your backside toward the chair and then walk backwards to the chair and guess when to sit (or keep peeking backwards)? Or, do you first walk directly to the chair then turn and sit? That's called motor planning. Really good motor planners are called slalom racers or jugglers. And the point is? Well, the point is that injury to the brain can affect sensory mechanisms as well as sensory input. And further, that may be seen as awkwardness. GIGO, garbage in, garbage out. Without adequate input data or processing of that data, even an intact motor system will appear faulty. In hemiplegia, due to middle cerebral artery blockage, the sensory region of the brain is right in the problem area. It could even be more involved than the motor area depending on the luck of having alternate branching blood vessels handy. Very typically, the sensory loss to the upper extremity is the more serious loss. It can be severe enough to not even register the limb as part of self. This is important. The hand is primarily a sensory driven part. No matter how good we make the arm or hand look, if sensory function is poor then function will be poor. The reverse issue is more interesting. No matter how bad the part looks, if sensory testing is found to be good, then any postural improvement or motor repair will be used to increase function. For many, transfers and releases in the upper extremity are to enable donning clothing - specifically to enable getting the arm to and the hand through a sleeve. For others it is to not stand out in a crowd because of a strange posture. A USA presidential candidate solved that by having a pen in his paralytic hand making the fixed posture appear contextual. Recent emphasis has been placed on an old idea. We know that motor function can be reassigned if young enough. How about sensory function? Eye patches have been used for years to promote weak side usage. Periods of good side restriction have been used to promote weak side usage and avoid the progressive lessening of weak side input. But how about weak side discrimination? Games that are based on detection and description are valuable. So, reach under the blanket and bring out the large block. Now find the nail file, not the popsicle stick. Which is the warm spoon? Things like that. Try to bring out discrimination. On that capability, rides success or failure. Because of the very fine discrimination and fine control of the hand, even equal sensory loss in the hand causes worse hand function than leg function. The most needed sensation from the foot relates to timing of walking and confirmation of single limb support integrity. When sensation is impaired, the timing will get inferred from other means. In tertiary syphilis, sensation in the legs is badly impaired with no loss in motor function. One can hear a syphilitic coming from way off by the loud slapping of the feet. The slapping isn't a defect in motor control but a means to detect when the feet have hit the ground - by sound. The eventual result is destroyed joints from injudicious repetative impact. A polio patient with very advanced muscle power loss often walks because the sensory side is normal and therefore compensatory tricks can be executed with precision. So in hemiplegia, with a pronated forearm (palm down) and a flexed wrist and thumb in palm might be much better postured for function with muscles transfers but might not do anything functionally better if sensory mechanisms are not there to modulate the intended new actions. That does not mean, don't do it. It means don't pin too much hope on postural solutions. Another oddity. In some inexplicable way, intact sensation figures in growth equalization between the two sides and between muscle components. When sensation is reduced, the part affected tends to undergrow by a small percentage. This may be the mechanism as to why some muscles undergrow in CP. Maybe. Mmmm. Maybe not. In any event, in hemiplegia, undergrowth of the affected side is far more parallel to the sensory loss than to the motor function difference between right and left. This is also true of bone density. There is a lot we don't know.