Chase's History
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~Born August 24, 2007 ~ 3 pounds 1 ounce, 5 weeks premature with intra-uterine growth restriction
At 3 weeks of age, while still in the Neonatal Intensive Care Unit Chase was diagnosed with Bilateral Optic Nerve Colobomas which has left him legally blind, with no treatment options
~ On September 24th Chase was released from the NICU at 3 pounds 15 ounces
Since being released he has been very involved with Early Intervention, receiving Vision Therapy and Special Education Instruction twice a week, Physical Therapy three times per week, Occupational Therapy twice a week and will soon start Speech Therapy
~ Chase has been hospitalized twice with RSV (respiratory syncytial virus) and twice with complications from vesicoureteral (kidney) reflux
Chase was labeled as having Cerebral Palsy in mid 2008
~ Doctors agreed, because of motor skills delays that an MRI was necessary in January of 2009
The results of the MRI showed not only mild Cerebral Palsy, but Cerebellar Hypoplasia, which means a small cerebellum, only in Chase’s case; his cerebellum is non existent and in its place is a pocket filled with fluid, they call this Absent Cerebellum
~ As a result, Chase will not walk without assistance, he is 17 months old and does not have the coordination to sit or stand without something to help him balance
Chase has no prognosis as of yet. This is so uncommon that the doctors need time to research and run more tests to try to find a definitive diagnosis
~ The assumption at this point is that Chase has some sort of genetic syndrome, if we can pinpoint a syndrome, we can better tell what to expect for Chase’s future.
Damage to the cerebellum can lead to: 1) loss of coordination of motor movement (asynergia), 2) the inability to judge distance and when to stop (dysmetria), 3) the inability to perform rapid alternating movements (adiadochokinesia), 4) movement tremors (intention tremor), 5) staggering, wide based walking (ataxic gait), 6) tendency toward falling, 7) weak muscles (hypotonia), 8) slurred speech (ataxic dysarthria), and 9) abnormal eye movements (nystagmus).
(www.neuroskills.com/tbi/bcerebel.shtml)
Complete absence of the cerebellum is an extremely rare malformation. Most previous cases have had some remnant of cerebellar cortex, however small.
(University of California, San Diego, Department of Pathology Neuropathology)
~Born August 24, 2007 ~ 3 pounds 1 ounce, 5 weeks premature with intra-uterine growth restriction
At 3 weeks of age, while still in the Neonatal Intensive Care Unit Chase was diagnosed with Bilateral Optic Nerve Colobomas which has left him legally blind, with no treatment options
~ On September 24th Chase was released from the NICU at 3 pounds 15 ounces
Since being released he has been very involved with Early Intervention, receiving Vision Therapy and Special Education Instruction twice a week, Physical Therapy three times per week, Occupational Therapy twice a week and will soon start Speech Therapy
~ Chase has been hospitalized twice with RSV (respiratory syncytial virus) and twice with complications from vesicoureteral (kidney) reflux
Chase was labeled as having Cerebral Palsy in mid 2008
~ Doctors agreed, because of motor skills delays that an MRI was necessary in January of 2009
The results of the MRI showed not only mild Cerebral Palsy, but Cerebellar Hypoplasia, which means a small cerebellum, only in Chase’s case; his cerebellum is non existent and in its place is a pocket filled with fluid, they call this Absent Cerebellum
~ As a result, Chase will not walk without assistance, he is 17 months old and does not have the coordination to sit or stand without something to help him balance
Chase has no prognosis as of yet. This is so uncommon that the doctors need time to research and run more tests to try to find a definitive diagnosis
~ The assumption at this point is that Chase has some sort of genetic syndrome, if we can pinpoint a syndrome, we can better tell what to expect for Chase’s future.
Damage to the cerebellum can lead to: 1) loss of coordination of motor movement (asynergia), 2) the inability to judge distance and when to stop (dysmetria), 3) the inability to perform rapid alternating movements (adiadochokinesia), 4) movement tremors (intention tremor), 5) staggering, wide based walking (ataxic gait), 6) tendency toward falling, 7) weak muscles (hypotonia), 8) slurred speech (ataxic dysarthria), and 9) abnormal eye movements (nystagmus).
(www.neuroskills.com/tbi/bcerebel.shtml)
Complete absence of the cerebellum is an extremely rare malformation. Most previous cases have had some remnant of cerebellar cortex, however small.
(University of California, San Diego, Department of Pathology Neuropathology)
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