– for the paralytic hip dislocation in the CP patient – a Salter osteotomy fails to address the problem of muscle imbalance, and initially the acetabulum is not really deformed anyways and does not need to be re-directed. Eventually, it may need some re-direction in which case a Dega is good to give them more posterior coverage.

– in Duchenne MD, the average IQ is lower. Myotonia is not part of this disease. Contractures are common, and the proximal muscles are affected first (typical of muscular dystrophies). It is inherited sex-linked recessive – the son evidently gets it from his mother (because he gets the Y from the father).

– the best time to biopsy a DMD muscle is when it still has some strength – grade 3. Waiting too long and it will only show fibrosis and fatty replacement.

– contractures are common with DMD

– a child with polio who puts his hand on his thigh to walk has week hamstrings, g. max, rectus femoris. The gluteus medius is probably not affected.

– in DMD, the son that is affected evidently gets it from his mother. Mom has 2 X chromosomes – one with the affected gene. Therefore, half of the daughters will be carriers.

– the key protein deficiency in DMD is dystrophin.

– the ideal CP hand surgical patient is motivated, intelligent, with good sensibility, and most importantly, demonstrates voluntary use of the extremity. Sensibility is assessed with stereognosis, graphesthesia, two point discrimination, and proprioception. The better the sensibility, the more useful the extremity. If you did an FCU to EDC transfer to achieve finger extension, I think a good result would be precluded if the patient did not have the voluntary ability to release grasp (ie. extend his fingers).

– an L3 level of spina bifida has the highest incidence of hip dislocation. Thoracics – 28%, L1/2 (high lumbar) – 30%, L3 – 36%, L4 – 22%, L5 – 7%, and sacral – 1%.

– if the L4 is intact, the spina bifida patient may develop a cavovarus deformity.

– DMD patients excrete excess creatinine in the urine.

– heel-cord lengthening and braces can prolong the ability of DMD patients to walk

– for a hemiplegic CP who has a passively correctable equinovarus deformity – can try an AFO (for the equinus) with a lateral T strap to pull the foot out of supination.

– in a CP patient who has a 20 degree adduction deformity and 25% uncovering of the femoral head – ie. it’s on its way out – do an adductor tenotomy +/- obturator neurectomy, plus femoral derotation varus osteotomy.

– there is a recurrent question about best indicator of prognosis for surgery of the hand in CP patient. The suggestion in a number of these answers is that sensation in the form of stereognosis and proprioception is the most important, but in reality, it seems as if voluntary use is the most important thing. Spasticity may limit voluntary use of the limb, and would seem to be a more important factor.

– treatment of dynamic equinus deformities should start with bracing (AFO) or BOTOX.

– the lowest level in spina bifida with cavus feet – L4 probably. L5’s get calcaneal valgus deformity

– clawtoes in the myelomenigocele patient come from a loss of intrinsics but functioning extrinsics

– a newborn L4 spina bifida will have cavus/varus feet; only 20% of spina bifida kids have normal feet at birth.

– in a polio patient with a drop foot but good plantar flexion – consider tib post transfer to dorsum of foot through interosseous membrane.

– beware the acute presentation of polio: listlessness, sore throat, vomiting, hyperesthesia, paresthesia, fever, severe headache, and an asymmetric paralysis or neurologic findings. Reflexes are absent in the muscle groups that are paralyzed. No objective sensory signs are noted (this is anterior horn disease). The most helpful lab procedure to diagnose polio would be spinal fluid cell count and protein level (unremarkable). In patients with upper extremity involvement, watch out for intercostals and diaphragmatic weakness, which may lead to severe respiratory embarrassment.


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