Maybe our French friends have the legal system right…rather than a blame game, maybe we should look into what happened.

The last article shows even the daddy of SBS has his concerns now, and mentions how experts on opposite sides won’t talk, know how sneaky and rude some of them are (not the CPS - some of them are very dirty)- the experts! You can say backstabbing in some cases!

So maybe we should look at ou system as its a joke. The way the Dowler family were treated, not sure if you had doors let go onto you by Police Officers and the CPS…that was fun. What happened to the Dowlers is disgusting but sadly will have gone on today and will go on tomorrow until we look at the bigger picture.

Maybe that would bail out a leaky system.

Which of course brings me to Bail…still wasted here…the T’Times, T’ Guardian, T’Telegraph and T’Inderpendant (Northern Editions) should snap me up before Viz do.

So the Police can’t bail people for longer than 4 days, no to be holisitic they need longer of course, tests take an age to come back, the CPS do, etc etc.

However…should they have people of Bail for a year or more…that can’t be right (been there) terrible abuse of family freedoms etc.  We had to wait and wait and wait (and Maeve’s family of course) all so experts could be given more time (and money)…to guess based on dodgy theory that the Father of SBS says wouldn’t ‘hang a cat’ on that evidence…

HMS Justice is sinking and if we are to save it, we need to help it out…pass the buckets  

So…

Yet another sea change, the SBS Guru changes heart…

Rethinking Shaken Baby Syndrome

by Joseph Shapiro

June 29, 2011

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June 29, 2011

The dispute over shaken baby syndrome is a bitter civil war. On one side, doctors, lawyers and other experts say the diagnosis is key to winning convictions of people accused of the most horrible acts of child abuse. Opponents say the diagnosis is used too freely and that sometimes, innocent people go to prison.

Norman Guthkelch, the pediatric neurosurgeon who is credited with first observing the condition in young children, is speaking out for the first time about his concerns regarding how that diagnosis is used. He worries that it is too often applied by medical examiners and doctors without considering other possible causes for a child’s death or injury.

Enlarge Courtesy of Norman GuthkelchNorman Guthkelch, a pediatric neurosurgeon who is credited with discovering shaken baby syndrome, is now having second thoughts about how the diagnosis is used in court.

 

Courtesy of Norman Guthkelch

Norman Guthkelch, a pediatric neurosurgeon who is credited with discovering shaken baby syndrome, is now having second thoughts about how the diagnosis is used in court.

Guthkelch, who is now 95, would like to play peacemaker. “There are cases where people on both sides, both of whom I admire equally, are barely able to speak to one another,” he says. “And that’s a shame.”

Guthkelch is concerned that there are too many cases like the one he recently reviewed in Arizona. A defense attorney asked him to look at the case of a father who has spent 10 years in prison after being convicted of killing his 5-month-old son by shaking him.

After reviewing the trial record and medical reports, Guthkelch said he was troubled to see that the medical examiner’s autopsy had concluded that the baby died of shaken baby syndrome while discounting other possible causes: A month prior to the child’s death, the boy had been admitted to the hospital with uncontrolled seizures. The baby had also briefly been in the neonatal intensive care ward after a difficult birth.

To Guthkelch, this suggests the boy may have instead died from natural causes. “I think I used the expression in my report, ‘I wouldn’t hang a cat on the evidence of shaking, as presented.’ ”

NPR teamed up with PBS Frontline and ProPublica and studied nearly two dozen cases in the U.S. and Canada where people were first convicted of killing children but later acquitted or had the charges dropped. Common patterns in these cases emerged over questionable autopsies and testimony, as well as disputes over medical evidence, such as the shaken baby syndrome diagnosis.

Diagnosing Shaken Baby Syndrome

Three years ago, Guthkelch received a standing ovation when he was introduced at the international conference of the National Center on Shaken Baby Syndrome.

“So who should be credited for discovering shaken baby syndrome? My vote is for Dr. A. Norman Guthkelch,” said Carole Jenny, a pediatrician with a specialty in child abuse prevention, as she introduced him to the group.

Jenny noted that Guthkelch wrote his groundbreaking paper in the British Medical Journal in 1971. It was just two pages long and called “Infantile Subdural Hematoma and its Relationship to Whiplash Injuries.” That paper, Jenny explained, “is the first clear, unambiguous reference in the world’s medical literature to shaking as a mechanism of head injury in infants and small children.”

Brithish Medical Journal: Infantile Subdural Hematoma And Its Relationship To Whiplash Injuries (PDF)

Guthkelch was trying to solve a medical mystery: Babies, toddlers and other children were showing up at his hospital with subdural hematomas — or bleeding on the surface of the brain — yet there were no signs of the cause. These children came with no broken bones, bruises or other signs of physical abuse.

He solved the mystery with a simple observation: In northern England, where he lived, parents sometimes punished their children by shaking them.

It was socially acceptable. “They had no motive to lie,” Guthkelch says. “So the parents told me the truth. ‘Yes, I shook him.’ ”

More From Our Post Mortem Investigation

Frontline: A Diagnosis Challenged

Q&A About The Child Cases’ Investigation

The Child Cases: Guilty Until Proved Innocent

Flawed work by forensic pathologists in pediatric death cases may be sending innocents to prison.

The Child Cases: Lessons From Canada

Tainted evidence accused a dozen people, such as Tammy Marquardt, of crimes they didn’t commit.

Post Mortem: Death Investigation In America

Unlike what you see on CSI, many suspicious deaths aren’t properly investigated.

At the same time, Guthkelch heard a revealing story from William German, a Yale University professor of neurosurgery. German told Guthkelch about a day he took his grandchildren to an amusement park. “They all went on the roller coaster and when it got to the summit of its travel, apparently it stopped violently and everybody was thrown quite violently,” Guthkelch explains.

A few days later, German developed bad headaches. He checked himself into the hospital where he worked and was found to have a subdural hematoma that required surgery. German figured it must have been caused by the violent jerk of the amusement park ride.

Guthkelch put these observations together and came up with his theory that a child could be shaken violently and develop bleeding on the brain — without any broken bones, bruises or other signs of physical abuse.

Controversy Among Medical Experts

Guthkelch’s chief concern was to inform parents about the dangers of shaking and to prevent abuse. And that’s still just as important today, he says. A baby’s brain is soft and surrounded by a thin skull, both of which can be easily damaged.

Other scientists built on his research. Now shaken baby syndrome is diagnosed when doctors find unexplained bleeding on the brain and two other symptoms: bleeding behind the retinas and brain swelling. This constellation of symptoms is referred to as “the triad.”

Too many medical experts see that triad of symptoms and conclude a child has been shaken without considering other possibilities, Guthkelch says. “I don’t think that the famous triad, however well some people think it’s defined, can ever be so well-defined that you can say that and nothing else cause it — that meaning shaking.”

In a case of measles, if you get the diagnosis wrong, in seven days’ time it really doesn’t matter because it’s cleared up anyhow. If you get the diagnosis of fatal shaken baby syndrome wrong, potentially someone’s life will be terminated

- Norman Guthkelch

Still, while shaken baby syndrome has been a widely accepted diagnosis for decades, a growing number of medical experts — particularly forensic pathologists — now question the diagnosis. Some skeptics cite research by biomechanical engineers that says you can’t shake a baby with so much force that you cause internal head injuries but leave no external marks, bruises or injuries to the neck or spine.

Others — including many pediatricians — strongly defend the diagnosis and say they often see its devastation. They say that violent shaking alone can cause a child’s death or severe brain damage with lifelong disabilities.

There are no exact numbers on shaken baby syndrome cases. The National Center on Shaken Baby Syndrome, a resource and advocacy group, estimates there are about 1,200 to 1,400 cases a year of severe or fatal head trauma from child abuse. The FBI reports about 500 homicides a year of children under the age of 5, from all causes.

Too Much Caution?

Not all experts share Guthkelch’s desire for new caution in diagnosing shaken baby syndrome. And some, like Teri Covington, who runs the National Center for Child Death Review Policy and Practice, worry that there’s already too much caution. She says that because of disputes over the science, there are growing cases of child abuse where the abuser isn’t punished at all.

Covington’s federally funded research center helps states investigate child deaths. And Covington says that when she meets with prosecutors, police and medical examiners, they say they’re already reluctant to bring even pretty clear cases.

“I have heard many a discussion of reluctance from both law enforcement and prosecutors to even start moving these cases forward in the way that they would have done five or 10 years ago,” she says.

Now, Covington says, many prosecutors won’t pursue cases unless they have a “definite whodunit” that can be proved easily in court. “I’ve seen that happen several times in the last few months,” she adds.

When Medicine Enters The Courtroom

Guthkelch says doctors need to be extra cautious when medicine reaches the courtroom. Medical knowledge changes over time, but the criminal justice system wants certainty to determine guilt or innocence. “In a case of measles,” he says, “if you get the diagnosis wrong, in seven days’ time it really doesn’t matter because it’s cleared up anyhow. If you get the diagnosis of fatal shaken baby syndrome wrong, potentially someone’s life will be terminated.”

That’s one reason Guthkelch says it’s time to get all sides together and try to agree on what can be said with scientific certainty about shaken baby syndrome.

At first he thinks perhaps a funder would sponsor a conference that would bring all the sides together. “If you have a spare couple million bucks and you’d like to finance a meeting, preferably in one of the good places like Vegas or Bermuda or whatever — then away we go,” he says with a laugh.

But then, on reflection, he thinks about the long-standing bitterness between all those competing doctors, lawyers, medical experts and child advocates. He says it’s important to have a civil dialogue — and almost a dream to think it can happen.

Hi, 

Found this on another site, just in case you missed it… 

Thursday, 2 June 2011

Forensic Science International Axonal Injury are NOT diagnostic of Trauma

 

A Local Authority v S Justice Eleanor King relied on Dr Al Sarraj and criticised Drs Cohen and Squier - looks like she was wrong and  relied on a doctor who really did have a polarised unscientific view! X Y and Z coming on this one!! Oh and looks like Keran Henderson has just been cleared doesn’t it! Who needs the Judges or lawyers any more eh! Just leave it to the scientists, the single journalist and the campaigner!

Triad + going out of that window!

 

Spinal nerve root β-APP staining in infants is not a reliable indicator of trauma.

 

 

Squier W^a  FRCP FRCPath (Corresponding author)

^aDepartment of Neuropathology

West Wing, John Radcliffe Hospital,

Oxford OX23 9DU

Email: waney.squier@clneuro.ox.ac.uk

Tel 01865 234932 Fax 01865 2321157

Scheimberg I ^b

^bDepartment of Cellular Pathology

Pathology & Pharmacy Building

Barts and the London NHS Trust

London E1 2ES

Smith, C MD FRCPath

Academic Department of Neuropathology, University of Edinburgh, Wilkie Building, Teviot Place, Edinburgh, EH8 9AG, UK

 

Ethics

This study has been undertaken with approval of the Local Research Ethics Committee (10/H0604/83) and the local NHS research governance regulations (Ref 6321).

 

Contributors

Dr Squier was responsible for the initial observations and planning the study. Dr Smith reviewed all the pathology and contributed to the preparation of the manuscript. Dr Scheimberg contributed to the preparation of the manuscript. All of the authors have approved the final manuscript.

 

Abstract

This preliminary communication describes seven babies with b- amyloid precursor protein (βAPP) positive axonal swellings in nerve root at multiple levels of the spinal cord. All seven babies died of natural causes. Two died in utero providing evidence for nerve root injury in the absence of trauma, two died within one day of birth and the possibility of birth related injury has to be considered. Three babies were over one month of age and had no history or pathological evidence of trauma.

These findings show that if axonal injury is carefully sought in every infant death, not just in babies where trauma is suspected, it will be found in a proportion of babies dying from natural diseases.  While spinal nerve root axonal injury in infants may suggest trauma, it is not, in itself, diagnostic of trauma.

Keywords: spinal nerve root, axonal injury, infant trauma, βAPP

 

 

Introduction

Axons are the processes arising from neuronal cell bodies and are involved in a constant flow of proteins, including βAPP, between the neuronal cell body and its peripheral synapses. Disruption of axonal flow is an indication of some form of axonal injury which may be metabolic, including ischaemic, or traumatic. Immunocytochemistry for b-APP is the most widely used marker of axonal injury in routine forensic neuropathology. The patterns demonstrated in adults using this marker may enable a diagnosis of diffuse traumatic axonal injury (TAI) (1), but there have been few studies to assess the patterns and incidence of TAI in the paediatric population. Indeed, studies of cases labelled as “non-accidental injury” have demonstrated that diffuse TAI is rare in infants, but they may exhibit focal brainstem axonal injury (2-4).

We are unaware of any detailed systematic study of nerve root injury at all levels of the spinal cord in adults or infants, whether due to trauma or any other cause. Two studies have referred to nerve root damage of the cervical spinal cord; Geddes (3) and Shannon (5) described damage to the cervical spinal cord and dorsal nerve roots in babies thought to have suffered non-accidental injury (NAI). Oehmichen (4) examined the cervical spinal cord in 5 cases of NAI and identified focal axonal injury in two.

There are rare mentions of nerve root injury in the absence of trauma; Shannon refers to axonal swelling in a single nerve root of a baby who drowned (5) and Dolinak noted axonal injury of the dorsal root entry zone in cases without any traumatic injury (6).

This preliminary communication is intended raise awareness of this issue by bringing attention to our observation of βAPP positive axonal swellings in spinal nerve roots in a group of neonates and in infants with no history of trauma. This is a matter of concern as it has been suggested that selective spinal nerve root expression of ß-APP is indicative of trauma (7).

Our observations highlight the need for detailed systematic studies of spinal cord pathology in the infant.

 

Material and Methods

During the course of routine diagnostic practice, seven babies were identified with nerve root swellings expressing ßAPP at multiple spinal levels. As this is suggested to be a diagnostic feature of trauma, these cases were reviewed.  Case details are set out in table 1.

Brains and spinal cords were fixed for between 10 days and 3 weeks in 10-20% formalin.  Sections were stained for ßAPP (Invitrogen) diluted 1/10,000 after endogenous peroxidase blockade and antigen retrieval by autoclaving and formic acid treatment. Stain was developed with Envision kit (Dako) and counterstained with haematoxylin.  

 

Results

In each of our cases clusters of axonal swellings expressing ΒAPP were seen in nerve roots at one or more levels of the spinal cord. ΒAPP positive swellings were identified in dorsal and ventral nerve roots and in nerve roots lateral to the cord as they united to cross the dura. (Figure 1).

Swellings were seen in axons both within the dural sheath and in extradural nerve roots, sometimes also in the dorsal root ganglia (Figure 2).  In one case the level and position of axonal swellings was not noted.

We saw well defined axonal swellings in an eighth case, a young child who drowned, but we do not have consent to use this case for research.

The majority of nerve roots did not express βAPP (Figure 1d).  

βAPP was frequently expressed in neuronal cell bodies of the spinal cord and was particularly strong in those of the dorsal root ganglia.

In some cases we noted congestion of nerve roots as they cross the dura, sometimes associated with extradural bleeding (Figure 3). 

Discussion

We have identified spinal nerve root axonal swellings in seven infants with no clinical or pathological evidence of trauma.  

Mechanical trauma and shearing may both cause interruption of axonal transport which results in swellings, beading and varicosities. Axonal swellings strongly express a number of immunohistochemical markers including b- amyloid precursor protein (b-APP), neurofilaments, and NSE; ßAPP is a widely used as a sensitive and specific marker of axonal injury (8). However, similar axonal swellings are seen in a variety of other conditions, including hypoxia-ischaemia and metabolic damage such as hypoglycaemia and carbon monoxide poisoning (1). In routine practice the commonest differential diagnosis lies between diffuse traumatic axonal injury and axonal injury secondary to global ischaemic injury.

Our results may be considered in two groups: babies who died before or shortly after birth and babies who died more than one month after birth.

 

Babies dying in the perinatal period

Two babies (cases 1 and 2) were stillborn and, as development of axonal swellings is a vital process, the axonal swellings in these babies must have been acquired prior to birth. These cases provide convincing evidence that birth trauma was not a cause of their axonal damage and generalised hypoxic-ischaemic injury is a likely cause.

Two babies (cases 3 and 4) died within one day of birth, one by vaginal delivery, the other by Caesarian section. In these babies the possibility of nerve root trauma during delivery becomes relevant.

The spinal nerve roots within the spinal canal are relatively protected from direct mechanical impact, but they may be subject to stretching and tearing if the spine is flexed abnormally. Cadaveric and animal imaging studies have shown that flexion of the spine causes stretching and medial displacement of the nerve roots of the cauda equina(9). In adult cadavers flexion of the trunk caused displacement of the cord of up to 1.8 cm, the maximum displacement being between cord levels C8 to T5 (10). These findings suggest that hyperflexion or extension of the head on the neck could be capable of causing nerve root traction at multiple spinal cord levels. Geddes (2) suggested that brainstem and cervical spinal cord damage may result from hyperflexion or hyperextension of the head on the neck, a mechanism proposed in shaking injury.

Cervical spinal cord damage has been described after both vaginal and caesarean deliveries (11). Brachial plexus nerve root injury usually occurs in malpresentations and after instrumental delivery and tends to be associated with shoulder dystocia, large babies and a long second stage (12). Some cases are due to an insult in utero and brachial palsy has been clearly documented in cases with no traction (13).

Case 3 was a vaginal delivery who was floppy at birth and survived 12 hours. There was no evidence of trauma. It may be suggested that a floppy baby may be more likely to succumb to the forces of delivery which would be transmitted to the neck if muscle tone is reduced. This hypothesis has not been tested.

Case 4 was a caesarean section with a forceps extraction associated with parietal skull fracture, which is clear evidence of trauma. Skull fractures represent 2.3% of birth injuries (14), they are more common in instrumental deliveries but can also be seen in spontaneous vaginal deliveries or caesarean sections (15). They may be caused by compression from forceps blades or from the skull pushing against the maternal pelvis (16). In case 4 trauma was probably due to compressive forces from forceps application and does not imply transmission of excessive hyperextension or hyperflexion forces to the neck or spine, but this cannot be excluded.

 

Babies dying after the perinatal period

None of the babies dying after 1 month after birth (cases 5-7) had either a clinical history or pathological evidence of trauma.  Causes of death were apnoea of unknown cause, myocardial infarction following heart surgery and spontaneous rupture of an intracranial aneurysm.

Axonal swellings may develop within 35 minutes of injury (17) and in the adult central nervous system occasional swellings have been identified up to 3 years after trauma (18;19). We do not know if these timings apply to infants as no study addresses this in this age group. As all of our cases were under 3 years of age we cannot be certain that the axonal swellings are not the result of birth-related trauma.

 A common factor in our older cases (5,6,7) was extensive, severe brain swelling. All had a clinical history of collapse and hypoxia and histological features of acute hypoxic-ischaemic injury (HII). The focal and patchy pattern of axonal injury we identified, with marked asymmetry between or within fascicles is characteristic of the pattern recognised in adult ischaemic peripheral nerve damage (20) and suggests this to be the likely cause.

Severe brain swelling may itself cause cervical nerve root injury by displacement and compression of the cervical spinal cord. Further distortion of the cervical cord and traction on cervical nerve roots may be seen if there is displacement of the cerebellar tonsils or masses of ectopic cerebellar tissue into the spinal canal, which is not uncommon in infants. None of our cases had brain swelling of this degree and in none of this series was there cerebellar displacement into the spinal canal.

 

Nerve root appearances

Axonal swellings were identified at multiple cord levels in most cases and were most common in the lateral roots where nerve bundles united to pass through the dural sleeve. Ventral nerve root swellings appeared to be more frequent than dorsal but no formal assessment was made in this preliminary study. Axonal βAPP expression was seen within the dorsal root ganglia in one case. In another case ganglion cells were seen among the intradural nerve roots and could be mistaken for axonal swelling on a cursory examination (Figure 2b).

In some nerve roots ßAPP expression was subtle, not associated with marked swelling and seen in only a few fibres. While unlikely to have been diagnosed as trauma by most pathologists, these mild appearances have been noted because confirmation bias may lower the threshold for diagnosis of axonal injury when faced with a case where trauma is suspected. This underlines the need for an objective analysis of spinal nerve root pathology in infants dying from all causes.

 

Nerve root congestion and haemorrhage

Some cases showed extensive congestion of the nerve roots as they cross the dura and in the adjacent epidural region.  These regions have an extensive vascular plexus involved in spinal fluid absorption (21).  Congestion and bleeding from the extensive vascular plexuses around spinal nerve roots may be related to changes in intracranial and abdominal pressure (22;23), is frequently seen in HII and is not a reliable indication of trauma.

 

Conclusion

It has been our experience that, if spinal nerve roots are routinely and carefully examined in babies dying from natural diseases, axonal pathology may be seen at all levels of the spinal cord in babies dying shortly after birth and in infants with no history or evidence of trauma. b-APP immunostaining in nerve roots is not, of itself, diagnostic of traumatic axonal injury.

Our evolving understanding of the distribution and significance of axonal injury in the brain has relied on detailed studies of b-APP immunostaining; similar studies are required to fully understand the pathology in spinal cord and nerve roots. The pathologist making a diagnosis based on this method must be aware that the expression of b-APP is only an indication of axonal dysfunction and is not diagnostic of mechanical trauma, such as axonal transaction, or irreversible damage.

This study is not systematic or exhaustive but serves to warn that caution is indicated in the interpretation of spinal nerve root injury in infants.  Axonal swellings per se, even at multiple cord levels, are not diagnostic of trauma.

 

Acknowledgements

We are grateful to all those parents who have given us consent to study the brains of their babies. Cases were sent for routine clinical diagnosis by Drs Colene Bowker, Stephen Gould, Irene Scheimberg and Liina Kiho. We thank Dr Steve Gould for his helpful commentary of the manuscript. We acknowledge the skill and dedication of the laboratory staff at the Department of Neuropathology at the John Radcliffe Hospital Oxford who carried out technical work and stained the sections.

 

Case Number	Age	Time since collapse	Cause of Death	Pathology	D/V/L	Level
1	35.40	-	Intracranial haemorrhage seen in utero. CS, stillborn.	Maceration Recent IVH and global HII. Old PVL Recent intravascular thrombosis.	D,V,L	T,S
2	37.40	Days-weeks	Polyhydramnios, Brain noted to be abnormal in utero. CS.	Old HII and widespread necrosis. Macerated baby, no evidence of trauma.	L	T
3	38.40	1d	Polyhydramnios. Floppy at birth. Seizures, possible metabolic disease	Recent global intrauterine HII. No evidence of trauma . No SDH.	D,V,L	T, L, S
4	40/40	12h	Emergency CS Birth asphyxia and birth trauma	Right  parietal skull fracture, subpial and subarachnoid haemorrhage. HII	D,V, L	T, L, S
5	1/12	3h	Multiple apnoeic episodes. Apnoea, collapse, resuscitated for 3h	Acute brain swelling and HII. Hippocampal microglial proliferation. No evidence of trauma no SAH or SDH	D,V	C , S
6	3 m	3d	In hospital collapse following  repair of CHD. Myocardial infarction	Recent global HII. No SDH	V	C, IIIn
7	9m	2d	Rupture of vein of Galen aneurysm	Global HII. Acute white matter necrosis (PVL)	Not recorded	Not recorded

 

 

 

 

 

Figure 1

1a: (Case 4) Section of lumbar spinal cord stained with βAPP. Even at low power nerve roots crossing the dura (d) can be seen to express this protein. There is diffuse staining of some white matter tracts and nerve cell bodies within the cord (Original magnification x 4).

1b: (Case 4) Higher power image of nerve roots crossing the dura in Figure 1a. Diffuse expression of βAPP is seen in many roots as well as groups of well defined swellings (Original magnification x 20).

1c: (Case 1) Sacral cord, patchy expression of βAPP in small groups of axons within a fascicle (Original magnification x 20).

1d: (Case 1) Thoracic cord, nerve roots are negative, but swollen axons expressing βAPP are seen at the periphery of the adjacent spinal cord (SC) (Original magnification x 20).

 

Figure 2

2a: (Case 2) Dorsal root ganglion at thoracic level. Ganglion cells are strongly positive as are a number of axons within the ganglion (Original magnification x 40).

2b: (Case 3) Sacral cord; two ganglion cells among nerve roots beneath the dura. Note strong positivity in ganglion cells and a few swollen axons in adjacent nerve roots (Original magnification x 20).

 

Figure 3

(Case 1) H&E stained section of thoracic spinal cord showing marked congestion and fresh subarachnoid and subdural (SD) bleeding and intradural congestion. Note the congestion of the nerve roots as they unite to cross the dura (arrows). This region is responsible for CSF resorption.

 

Reference List

 

  (1) Reichard RR, Smith C, Graham DI. The significance of beta-APP immunoreactivity in forensic practice. Neuropathol Appl Neurobiol 2005 Jun;31(3):304-13.

  (2) Geddes JF, Vowles GH, Hackshaw AK, Nickols CD, Scott IS, Whitwell HL. Neuropathology of inflicted head injury in children. II. Microscopic brain injury in infants. Brain 2001 Jul;124(Pt 7):1299-306.

  (3) Geddes JF, Hackshaw AK, Vowles GH, Nickols CD, Whitwell HL. Neuropathology of inflicted head injury in children. I. Patterns of brain damage. Brain 2001 Jul;124(Pt 7):1290-8.

  (4) Oehmichen M, Schleiss D, Pedal I, Saternus KS, Gerling I, Meissner C. Shaken baby syndrome: re-examination of diffuse axonal injury as cause of death. Acta Neuropathol 2008 Sep;116(3):317-29.

  (5) Shannon P, Smith CR, Deck J, Ang LC, Ho M, Becker L. Axonal injury and the neuropathology of shaken baby syndrome. Acta Neuropathol (Berl) 1998 Jun;95(6):625-31.

  (6) Dolinak D, Reichard R. An overview of inflicted head injury in infants and young children, with a review of beta-amyloid precursor protein immunohistochemistry. Arch Pathol Lab Med 2006 May;130(5):712-7.

  (7) Royal College of Pathologists. Report of a Meeting on the Pathology of Traumatic Head Injury in Children.  2009.

  (8) Sherriff FE, Bridges LR, Gentleman SM, Sivaloganathan S, Wilson S. Markers of axonal injury in post mortem human brain. Acta Neuropathol 1994;88(5):433-9.

  (9) Bauer DF, Shoja MM, Loukas M, Oakes WJ, Tubbs RS. Study of the effects of flexion on the position of the conus medullaris. Childs Nerv Syst 2008 Sep;24(9):1043-5.

(10) REID JD. Effects of flexion-extension movements of the head and spine upon the spinal cord and nerve roots

1. J Neurol Neurosurg Psychiatry 1960 Aug;23:214-21.

(11) Goetz E. Neonatal spinal cord injury after an uncomplicated vaginal delivery. Pediatr Neurol 2010 Jan;42(1):69-71.

(12) Zafeiriou DI, Psychogiou K. Obstetrical brachial plexus palsy. Pediatr Neurol 2008 Apr;38(4):235-42.

(13) Pollack RN, Buchman AS, Yaffe H, Divon MY. Obstetrical brachial palsy: pathogenesis, risk factors, and prevention. Clin Obstet Gynecol 2000 Jun;43(2):236-46.

(14) Hughes CA, Harley EH, Milmoe G, Bala R, Martorella A. Birth trauma in the head and neck. Arch Otolaryngol Head Neck Surg 1999 Feb;125(2):193-9.

(15) Heise RH, Srivatsa PJ, Karsell PR. Spontaneous intrauterine linear skull fracture: a rare complication of spontaneous vaginal delivery. Obstet Gynecol 1996 May;87(5 Pt 2):851-4.

(16) Doumouchtsis SK, Arulkumaran S. Head injuries after instrumental vaginal deliveries. Curr Opin Obstet Gynecol 2006 Apr;18(2):129-34.

(17) Hortobagyi T, Wise S, Hunt N, Cary N, Djurovic V, Fegan-Earl A, et al. Traumatic axonal damage in the brain can be detected using beta-APP immunohistochemistry within 35 min after head injury to human adults

1. Neuropathol Appl Neurobiol 2007 Apr;33(2):226-37.

(18) Geddes JF. What’s new in the diagnosis of head injury? J Clin Pathol 1997 Apr;50(4):271-4.

(19) Chen XH, Johnson VE, Uryu K, Trojanowski JQ, Smith DH. A lack of amyloid beta plaques despite persistent accumulation of amyloid beta in axons of long-term survivors of traumatic brain injury. Brain Pathol 2009 Apr;19(2):214-23.

(20) Fujimura H, Lacroix C, Said G. Vulnerability of nerve fibres to ischaemia. A quantitative light and electron microscope study. Brain 1991 Aug;114 ( Pt 4):1929-42.

(21) Zenker W, Bankoul S, Braun JS. Morphological indications for considerable diffuse reabsorption of cerebrospinal fluid in spinal meninges particularly in the areas of meningeal funnels. An electronmicroscopical study including tracing experiments in rats. Anat Embryol (Berl) 1994 Mar;189(3):243-58.

(22) Takiguchi T, Yamaguchi S, Tezuka M, Furukawa N, Kitajima T. Compression of the subarachnoid space by the engorged epidural venous plexus in pregnant women. Anesthesiology 2006 Oct;105(4):848-51.

(23) Su CS, Lan MY, Chang YY, Lin WC, Liu KT. Clinical features, neuroimaging and treatment of spontaneous intracranial hypotension and magnetic resonance imaging evidence of blind epidural blood patch. Eur Neurol 2009;61(5):301-7.

 

 

http://www.familylawweek.co.uk/site.aspx?i=ed53850

84. Dr. Al-Sarraj also examined the spinal cord. The axon is a nerve fibre which connects other nerve cells. They are generally in bundles. Protein comes down the fibres. One of the proteins is ßAPP i.e. Beta-Amyloid Precursor Protein. If the axon is damaged for any reason, normal transmission will be interrupted and beads or swelling may be found along it. Such observations can be used as an indicator of damage, if deposition is seen in the spinal nerve roots it raises the possibility of traumatic root damage.

85. The identification of such damage does not in itself tell a neuropathologist whether the cause of the damage is due to ischemia or trauma. Multiple deposits were seen in the anterior horn cells (this is grey matter with nerve cells within the spinal cord itself) that is complimentary to a finding of ischemia. To Dr. Al-Sarraj of particular significance, however, is the ßAPP stain deposition seen in the spinal nerve roots which are found outside the actual spinal column.

86. At the top of the spinal cord, at the cervical segment, Dr. Al-Sarraj found a heavy deposition. At the thoracic segment there was a focal deposit in a few posterior spinal root nerves and in the lumbar region very occasional small deposits in one or two posterior spinal roots.

87. Due to the fact that these depositions in the spinal nerve roots are mainly in the posterior aspect and focal, rather than throughout the spinal cord, this raised the possibility to Dr. Al-Sarraj of the possibility of traumatic axonal damage. Although ischemia (which was seen throughout the spinal cord), could not be completely excluded as the cause of an axonal injury, it was, he said, also possible that it was the consequence of the movement of the spinal cord and stretching of the nerve roots in shaking. In other words, a hyper-flexion, hyper-extension injury.

88. ßAPP examination in the cranial nerve roots of the brain was carried out. This is done routinely. Although there is no peer reviewed literature as yet published, this is an area of research in which Dr. Al-Sarraj’s department is engaged. Damage in that location would tend to favour ischemia and in Z’s case there was no evidence of axonal damage in the cranial nerve roots. When the cranial nerves are not involved and only local and posterior spinal nerves, whilst you cannot totally exclude ischemia as the cause, it is more likely, Dr. Al-Sarraj said, to be due to trauma.

Posted by Penny Mellor at 08:58 0 comments

Or also known as when?

OOOh there was something in Scotland….

Anywhere else?

I know we don’t have much left, just saw pictures of our carrier being cut up in Turkey…

So we could only probably manage a few to Scotland…but come on, I see more troops on Top Gear, mind you maybe they are just stunt doubles or extras? We can’t have that many left… 

We did a little something at the weekend in my nod of the head to comrades still in the services. But it is sad how little it means and is plugged or not.

Oh and Mr Cameron, you may want to rethink sneaking bodies out of the back door at Brize Norton, that will come back and bite you on the arse.

The people who go to Royal Wotton Bassett will go there and MAKE it an event, so if it is deliberate, change it, if not then make sure its seen to be re thought asap.

I know it bad PR having all those dead troops come back, it will be a million times worse if you hide it or allow it to be hidden by someone who thinks you want it hidden.