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Low Pressure HBOT

Harch HBOT in Cerebral Palsy and Pediatric Neurology: A Scientific Perspective

This article will review the current literature and history of application of low pressure (low dosage) LPHBOT to pediatric neurology. The most rigorous study on this subject will be analyzed and its interpretation debated in terms of past and present scientific data and theoretical considerations. The major flaw in the study's conclusion is illustrated by pre and post HBOT SPECT brain imaging on two of the author's cerebral palsy patients and the author's 12-year-experiehce of HBOT treatment of Cerebral Palsy children. There is substantial scientific explanation and data to argue for reimbursement of HBOT in Cerebral Palsy.

Hyperbaric Oxygen Therapy in the Management of Cerebral Palsy

HBOT in the Management of Cerebral Palsy

Virginia Neubauer, Richard Neubauer and Paul Harch

 

An entry from K.K. Jain's Textbook Of Hyperbaric Medicine

Cerebral palsy is a chronic neurological disorder that can be due to several causes of brain damage in utero, in the perinatal period, or postnatally. Hyperbaric oxygen has been shown to be useful in treating children with cerebral palsy. This topic is discussed under following headings:
Causes of Cerebral Palsy
Oxygen Therapy in the Neonatal Period
Treatment of Cerebral Palsy with HBOT
Conclusions

 

Causes of Cerebral Palsy
 

The term cerebral palsy (CP) covers a group of non-progressive, but often changing, motor impairment syndromes secondary to lesions or anomalies of the brain arising in the early stages of development. Between 20 to 25 of every 10,000 live-born children in the Western world have the condition (Stanley et al 2000). Problems may occur in utero, perinatal, and postnatal. Infections, traumatic brain injury, near-drowning and strokes in children suffering from neurological problems come under the heading of cerebral palsy. Diagnosis of cerebral palsy resulting from in utero or early perinatal causes may be made immediately after birth, but more commonly occurs between 15 and 24 months. It is possible that CP may be misdiagnosed for years because specific symptoms may show up very late in childhood. Some of the possible causes of Cerebral Palsy and are listed in Table 21.1.
Although several antepartum causes have been described for CP, the role of intrapartum asphyxia in neonatal encephalopathy and seizures in term infants is not clear. There is no evidence that brain damage occurs before birth. A study using brain MRI or post-mortem examination was conducted in 351 full-term infants with neonatal encephalopathy, early seizures, or both to distinguish between lesions acquired antenatally and those that developed in the intrapartum and early postpartum period (Cowan et al 2003). Infants with major congenital malformations or obvious chromosomal disorders were excluded. Brain images showed evidence of an acute insult without established injury or atrophy in (80%) of infants with neonatal encephalopathy and evidence of perinatal asphyxia. Although the results cannot exclude the possibility that antenatal or genetic factors might predispose some infants to perinatal brain injury, the data strongly suggest that events in the immediate perinatal period are most important in neonatal brain injury. These findings are important from management point of view as HBOT therapy in the perinatal period may be of value in preventing the evolution of cerebral palsy.