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Motor abnormalities that have had their onset early in life are numerous and diverse in their clinical manifestations Marked prematurity is a determining factor in a large proportion of cases Each year, about 50,000 infants weighing less than 1500 g are born in the United States Approximately 85 percent survive Of these, 5 to 15 percent have a motor disorder of cerebral origin and 25 to 30 percent are found to be mentally impaired at school age (Volpe; see also Hack et al) To ascertain the etiologic and pathogenic factor(s), it is helpful to categorize a given case according to the extent and nature of the motor abnormality A careful history of possible prenatal, perinatal, or postnatal insults to the developing nervous system must always be sought; certain correlations of these factors with the resulting pattern of neurologic de cit are outlined below.

will not be the center of attention, so moving the joystick will be easy to do without being noticed. Using all six servo channels, you could rig up an

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Most patients with these motor abnormalities of infancy and childhood reach adult years Many but not all have some degree of mental retardation and epilepsy in addition to the motor abnormalities, and there is an unavoidable overlapping in considering the causes and mechanisms of these three clinical states The following discussion of these problems is centered on the three major etiologic syndromes matrix hemorrhages in the immature infant, hypoxic-ischemic encephalopathy (Little disease), and certain developmental motor abnormalities Germinal Matrix (Subependymal) Hemorrhage in Premature Infants In low-weight and premature immature infants (20 to 35 weeks gestational age), there sometimes occurs, within a few days after birth, a catastrophic decline in cerebral function, usually preceded by respiratory distress (hyaline membrane disease), with spells of cyanosis and apnea Also evident are failure of brainstem automatisms (sucking and swallowing), bulging of the fontanels, and appearance of sanguineous CSF.

Orient the IC correctly into the socket, while referring to the schematic and layout diagrams. Place the IC into the socket. The receiver loop coil at L1 can be either the 800 turn coil wound on a plastic form, an old high impedance relay, or one of the black plastic suction cup-telephone pickup devices. Solder the coil in place between the circuit ground and the capacitor at C1. You could also elect to use a second 1/8 phone jack to allow the coil to be plugged into the circuit using a 6 to 8 length of coax cable. The volume control used for the prototype was a chassis mounted miniature 10k ohm potentiometer. We used a mini 1/8 PC style phone jack on the circuit board at the output of the audio amplifier at C6; this will allow you to plug in a headphone for listening. Take a short well deserved rest and when we return we will check the circuit board for possible short circuits and cold solder joints. Pickup the circuit board with the foil side of the circuit board facing upwards toward you. Look the circuit board over carefully to see if there are any cold solder joints. The solder joints should look clean, smooth and shiny. If any of the solder joints look dull, or blobby, then you

If the infant becomes completely unresponsive, death usually ensues within a few days Autopsy discloses a small lake of blood in each cerebral hemisphere (often asymmetrically distributed), occupying the highly cellular (subependymal) germinal matrix zone, near the caudate nucleus at.

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Generalized or universal paralysis: limb (but usually not cranial) muscles, involved either in attacks or as part of a chronic persistent, progressive deterioration When acute in onset and episodic, this syndrome is usually a manifestation of familial hypokalemic or hyperkalemic periodic paralysis One variety of the hypokalemic type is associated with hyperthyroidism, another with hyperaldosteronism (Chap 54) Attacks of porphyric neuropathy and of Refsum disease have an episodic nature Generalized paresis (rather than paralysis) that has an acute onset and lasts many weeks is at times a feature of a severe form of idiopathic or parasitic (trichinosis) polymyositis and rarely of the toxic effects of certain pharmaceutical agents, particularly those used to treat hypercholesterolemia Idiopathic polymyositis and rarely inclusion body myositis may involve all limb and trunk muscles but usually spare the facial and ocular muscles, whereas the weakness in trichinosis is mainly in the ocular and lingual muscles.

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