Brain Disorders / Neurological White Matter


The white matter is those areas of the nervous system rich in axons (electrical wires, for want of a better term) along which messages travel.

These messages can be related to movement, sight, etc. The axons are covered with glial cells. The glial cells are supportive cells, producing the lipid substance called myelin, which forms an insulating sheath around certain nerve fibers. The myelin can be likened to the colored plastic insulation we see around electrical wires. The messages (which can be likened to an electric current) travel down the axons, and the myelin helps keep the signal from becoming mixed up in the other axon pathways.
Different parts of the nervous system appear grey, white, or mottled. The grey matter is made up of a mix of cells and capillary blood vessels and, as its name implies, has a grey appearance. The connections between the cells are the axons (as described above) which are covered in glial cells. The glial cells, being fatty, have a high refractive index and appear white. An area of the brain rich in these is called the white matter. A part of the brain which is a good mix of cell bodies and axons (grey and white matter) is called the reticular formation as it has a netlike appearance.

White Matter, by James MD (Continued)

It would be better to refer to the outgrowths of neurons as simply fibres, because some are axons - where the signal is carried away from the cell and others are dendrites - which carry impulses towards the cell. Those fibres that are myelinated have segments, which are covered by a wrap of myelin sheath, which is the projection of the parent cell body - the oligodendrocyte. A single parent oligodendrocyte may be responsible for up to 20 myelin segments, which are organised like the tentacles of an octopus. The wrap is like a Swiss roll, with as many of 30 turns of sheath. The sheaths abut at the nodes of Ranvier. Conduction is along the sheath and is known as "saltatory." A non myelinated fibre may conduct at say 0.5 meters a second where a fully myelinated fibre of the same size may conduct at 150 mps. Insulation from cross talk is provided by cerebrospinal fluid, which is rich in surfactant, which absorbs to the surface of the sheath, and being a Zwitterion is strongly charged.

Although rarely acknowledged fibres in grey matter may also be myelinated. The oligodendrocyte has a very high metabolic rate and the sheaths are easily damaged by edema where there is protein extravasation probably due to complement activation.

Best wishes,

Philip James
Wolfson Hyperbaric Medicine Unit
University of Dundee

Hyperbaric oxygen treatment decreases post-ischemic neurotrophin-3 mRNA down-regulation in the rat hippocampus.

Yang JT, Chang CN, Lee TH, Lin TN, Hsu JC, Hsu YH, Wu JH.

Department of Neurosurgery, Chang Gung Memorial Hospital, Taipei 105, Taiwan.

The therapeutic effect of hyperbaric oxygen (HBO) on ischemic injury was investigated using in situ hybridization to detect the mRNA expression of neurotrophin-3 (NT-3), which is thought to play a crucial role in protecting against neuronal death induced by brain ischemia. The rats under investigation were subjected to 10 min transient forebrain ischemia, and subsequently exposed to HBO (100% oxygen, 2.5 atm absolute) for 2 h. Levels of NT-3 mRNA in the CA1, CA2 and CA3 regions, and the dentate gyrus of the hippocampus were measured after various reperfusion periods. Neuronal death in the hippocampal CA1 region was also measured by Nissl staining, seven days post ischemia. The results demonstrated that HBO treatment significantly reduced the ischemia-induced down-regulation of the NT-3 mRNA level at 4 h post ischemia, and significantly increased cell survival 7 days after reperfusion. The findings suggest that an HBO treatment maintaining the NT-3 mRNA level in the hippocampus can be beneficial to the ischemic brain within a certain time frame.

Studies for brain Damage and HBOT
Neubauer, RA et al. (1994). Hyperbaric Oxygen for treatment of closed head injury. Southern Medical Journal, vol. 87, #9, p 933-36.

Neubauer, RA et al. (1990). Enhancing idling neurons. The Lancet; vol 335, p542.

Holbach KH et al. (1978). EEG analysis for evaluating chronic cerebral ischemia treated by HBO and microneurosurgery. Journal of Neurology; vol 219,p227-240.

Haapaniemi et al. (1998). HBO treatment enhances regeneration of the rat sciatic nerve. Experimental Neurology; vol 149, p433-438.

Omae, T et al. (1998). Effects of high atmospheric pressure & oxygen on middle cerebral blood flow velocity in humans measured by transcranial doppler. Stroke; vol 29, p94-97.

Rockswold, GL et al. (1992). Results of a prospective randomized trial for treatment of severely brain-injured patients with HBO. J. Neurosurg.; vol 76, p929-934.

Holbach KH et al. (1977) Cerebral energy metabolism in patients with brain lesions at normo and hyperbaric oxygen pressures. J. Neurol.; vol 217, p17-30.

Neubauer, RA & James, P (1998). Cerebral oxygenation and the recoverable brain. Nerol Res; vol 20 (suppl 1), p 33-36

Hyperbaric oxygenation:

The recoverable brain in certain pediatric patients S.P.E.C.T. Brain Scans

Ocean Hyperbaric Center, Lauderdale-by-the-Sea, FL (USA)
* Department of Nuclear Medicine
Santa Monica-UCLA Medical Center, Santa Monica, CA (USA)
** The Hyperbaric Oxygen Trust
Forest Row, England, (UK) and the University of Dundee, Scotland


Anoxic-ischemic encephalopathy and traumatic brain injury in children are examples of devastating conditions which can be responsible for decades of disability. A regimen of single photon emission computerized tomography (SPECT) scanning and hyperbaric oxygen (HBO) treatment is now available to identify recoverable (stunned or dormant) brain tissue and potentially improve function in such patients. A baseline scan is performed. A challenge with hyperbaric oxygen ( 1.5 ATA, I Hr. 1-20 txs) is given and the scan is repeated. Observation of increased flow is indicative of increased metabolism since the tracer crosses the blood brain barrier. Such positive changes seen in the SPECT are frequently paralleled with clinical improvement. PT, OT, speech, biofeedback, occasional herbal medications are used as part of a multi-disciplinary brain repair approach. Three such cases will be presented, two cerebral palsy (M ages 3 and 4) and a F age 8, with closed head injury.
The protocol is one that had been previously published (1). It involves sequential SPECT (brain) functional imaging with an HBO challenge of (I hr x 1.5 ATA) 1-2 times a day in a monoplace hyperbaric chamber (dickers Ltd, Hampshire, UK). 1020 exposures to HBO were performed to ascertain the possibility of recoverable brain tissue. The second scan was done within two hours following the HBO exposure prior to the second scan. The radioactive tracer used was Tc 99m dl
Ljubljana, Slovenia 13-18 September 1998

These three patients illustrate the different patterns of mid brain damage from hypoxia/ischaemic insults and the effect of oxygen therapy
(Unfortunate lnadequate / Delayed).

Patient 1.

1992 Mid brain damage with spastic quadriplegia after carbon monoxide poisoning.
Female 39 attempted suicide sometime after midnight by locking herself in a hall cupboard with the exhaust from a small motorcycle piped in. Found at 2.30 a.m. she was admitted to a hospital ICU, given 100% oxygen and ventilated. Off the ventilator after 24 hours she was admitted unconscious to a ward for general nursing care. On the third day the clinician-in-charge referred her for hyperbaric oxygen therapy. She recovered consciousness in the first session. She had recall of events and became fully aware and communicative after six sessions. There was limb flaccidity and she developed a spastic quadriplegia over the following weeks.
She is now completely lucid and in long-term care. All four limbs have developed severe contractures.


From what we now know we should have continued treatment.
1998 Strangulation with asphyxia and carotid artery compression.
Male aged 27 suicide attempt in prison on remand using the cord from his boxer shorts. Period of hanging said to be 10 minutes. Admitted to ICU, ventilated via tracheostomy for two weeks and started opening his eyes. Thrashing ? athetoid movements of his limbs developed. After weaning of the ventilator, but with the tracheostomy still in place, he was transferred to Dundee. Hyperbaric oxygen therapy requested by the clinician-in-charge after four weeks when the neurologist noticed improvement in his EEG. The tracheostomy had been closed on the advice of the anaesthetist. A gastrostomy tube was inserted but was obstructing. His general condition was poor and he was very emaciated with abrasions and sores on his ankles, knees and elbows from friction with his bed. This was despite extensive padding. His lips were cracked and swollen. Only six hyperbaric oxygen treatments (1.75atm abs for one hour daily) were given after grommets were inserted. His general condition improved dramatically with healing of the sores. His lips healed. He had started to follow staff and make sounds. On the evening of the sixth day he aspirated and died.


Obvious comments about airway maintenance but he staff were astounded to see the general improvement despite inadequate nutrition. The only change in his management was some more oxygen 1999 Cardiac arrest of 30 minutes with defibrillation. Male aged 46 had a cardiac arrest in the community. Defibrillated by paramedics after about 30 minutes. Admitted to CCU and opened his eyes after three days. He began to say single words on day 5. Transferred to general ward on day 6. Gradually declined over 5 weeks with the development of spastic paraplegia, despite daily physiotherapy. Prescribed Lioresol. Slow improvement in mentation. His leg spasticity became so severe that it was very difficult to bend his legs to allow him to use a wheel chair. His arms were also developing mild stiffness. He had periods in which he spoke words clearly, but they made little sense. He recognised his family. Hyperbaric oxygen therapy was started after 5 weeks. A total of 54 daily, one hour, hyperbaric oxygen sessions were undertaken at 1.75 atm abs. His cognition and speech improved and there was dramatic improvement in his spasticity. He left hospital walking without assistance.
This illustrates Ischaemia with mid brain oedema. Giving high dosage oxygen post arrest would ? on present evidence- have prevented the associated the reperfusion injury and spared some of the cortical damage.

Best wishes to all

Philip James
Wolfson Hyperbaric Medicine Unit
University of Dundee

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