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xx Alan Stanford on CROOKNECK (from injury to head)
« Thread started on: Oct 15th, 2006, 10:44am »

Here is a video showing the condition:
http://www.youtube.com/watch?v=SS64ne2boQ0

The following "case study" includes the treatment article for CROOKNECK due to injury to the head (occurs quite often in SILKIES and other crested fowl)
reposted here with the relevant "HOLE-IN-HEAD" article from Alan Stanfords excellent article base at his site BROWN EGG BLUE EGG:
http://www.browneggblueegg.com/Article.html
THANKS Alan for your generosity and knowledge in sharing this!

Hi everyone,
> I think that one of my little birds is sick or getting sick. She seems fine as far as eacting or drinking, but she stumbles when she walks, and when you pick her up to pet her, she tucks her head in at a very wierd angle. I know that I've read symptoms like this on the list, just can't find the info - can someone help me out? What do I giveher, and do I give the other two the same? Thanks for all the help!!
Amy


Amy,
This can be many things.
The first things to check on chickens are lice, mites, and coccidiosis. These
can sap the strength of a bird and cause all sorts of symptoms. What's more,
all 3 of these are typically much worse on just a few birds in a flock. The
others have at least limited resistance. Yes, it is true, limited resistance
to lice and mites!

After that it sounds like a neurological problem.

One possibility is botulism or toxins from mold. Just a bit of moldy grain or fungus on the underside of floor boards, in bedding, or one walls can be the cause.

Another possibility is what I call crookneck. Silkies have a hole in the top of their skull and brain bulges out. A bow to this exposed brain can kill or cause
crookneck. The symptoms of crookneck include
1. Tucking the head between legs
2. Tucking the head between legs and backing up
3. Tucking the head between legs and tumbling over
4. Walking in circles
5. Holding the head to one side
6. Loss of balance

I have a treatment for crookneck that I will append to this email. Remember that I am not a vet and the best bet is to take my information to a vet. The prednisone in my treatment was suggested by a vet who did a necropsy on a Silkie with crookneck. He saw ‘water on the brain.”

In my treatment, the most important part is to hand feed if necessary and keep
the bird from harm from the other birds. The vitamins and prednisone will not
harm a bird with a different problem.

Alan

Treating "Crookneck"
by Alan Stanford
Permission to share this is granted as long as you give credit to the Author

Here is my theory and therapy for what some call "limber neck" and I call crookneck. The symptoms first show as a crook in the neck. It progresses to
tucking the head, then tucking the head between the legs, then backing up, and tumbling over. It usually hits young birds but can happen at any age.

It is unclear what causes crookneck. American Silkie Bantam Club members suggest water on the brain, vitamin E deficiency, and injury to the brain that
is outside the skull and forms the knob on the top of Silkie's heads. The brain injury is the cause I feel fairly certain about.

Water on the brain was seen in a necropsy of an affected bird. Prednisone was suggested as symptomatic relief. Vitamin E and B complex are both good for neurological disorders. Selenium helps absorb vitamin E.

Here's what I do for affected birds. If started before symptoms get severe, the bird will totally recover. To give vitamin E - just cut the end off a human capsule and squirt it in the bird's mouth.

It is important to be sure the bird gets enough to eat and drink while it has this problem. Birds with severe cases of crookneck can't eat and drink enough to survive. You will need to gently place their head in the feed dish and carefully dip just the tip of the beak in water. Be careful not to dip too far into the water and to not stress the bird while trying to help.

The following is for an adult about 2 pound bird. Scale back for smaller birds.

For the first week I give

Twice a day
2.5 mg of prednisone
400 IU of vitamin E

Once a day
A piece of human vitamin B complex pill or a squirt of human liquid vitamins
Selenium (50 micrograms/day for half size juvenile for 3 days)

For the second week I give

Once a day
2.5 mg of prednisone
400 IU of vitamin E
A piece of human vitamin B complex pill or a squirt of human liquid vitamins

Every other day
Selenium (50 micrograms/day for half size juvenile for 3 days)

For the following weeks I give

Once a day
2.5 mg of prednisone
400 IU of vitamin E
A piece of human vitamin B complex pill or a squirt of human liquid vitamins

Every third day
Selenium (50 micrograms/day for half size juvenile for 3 days)

Do not abruptly stop prednisone, the swelling rebounds, decrease dose
gradually.
Vitamin E recovery can be slow; continue the vitamin E for several weeks at
least.

You can get the prednisone from a vet; just describe the problem of
swelling in
the brain probably due to injury. Yes Silkies' brains do stick out through a
hole on the top of the skull.

You can get the vitamin E, selenium, and vitamin B complex or liquid
vitamins at
any pharmacy.

To get prednisone, print the pictures at
http://www.browneggblueegg.com/HoleInHead.html
and take them to a vet. (for those unable to access this article, Alan has generously given his permission to repost the article/photos below)

Silkies Have a Hole in Their Head
By Alan Stanford, Ph.D.
January 30, 2003

Silkies have a hole in the top of their skull. Kate learned this as she and a professor from the University of Wisconsin dissected a Silkie. As far as we know all Silkies have this hole in the head; perhaps the size varies from bird to bird. Our local vet claims there are other breeds with this odd feature.

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Many breeders select for Silkies with a knob on the top of their head because they believe knobs give larger and rounder crests. This knob is brain bulging outside the skull. We call birds these birds round heads and birds without knobs flat heads. Although we do not select for the knob, our friend George Mihalik found 90% of our show birds had round heads. Maybe there is some truth to the theory of round heads having better looking crests; maybe round heads are a dominant trait.

I have heard several stories of Silkies dieing from seemingly insignificant blows to the head. In 2001 Pedro (one of our cockerels) jumped and hit his head in a travel carrier. He died within an hour. After the 2002 Ohio National we found Attila the Hun (another of our cockerels) almost dead in a travel coop but I revived him with mouth to beak resuscitation. We guess he hit his head. I almost killed Attila a month later as I broke up a cockerel fight but once again I resuscitated him. I theorize that what we call crookneck and others call limber neck is caused by trauma to a Silkie's exposed brain.

Birds with crookneck tuck their heads between their legs and their neck muscles are taught. In severe cases the birds back up, twitch their tucked heads side to side, and flip upside down.

A necropsy of one of Valerie Hirvela's birds with crookneck found nothing except some fluid on the brain. The vet suggested prednisone might help afflicted birds. Vitamin E and vitamin B complex seem to help Crookneck birds; these vitamins help the nervous system. All of this is consistent with my theory that an injury to a Silkie's exposed brain produces crookneck. Crookneck strikes birds of any age. I think I saw a correlation with more crowding of our chicks. I also suppose raising Araucanas with our Silkies produced more crookneck birds. I speculate that the feisty Araucanas were popping the Silkies on the head.

Although the connection between crookneck and the exposed brain is only a supposition, the exposed brain is a fact.
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Here is an interesting link about the subject.
http://www.halcserver.com/beebe/science.html

(scroll down to >Crested fowl - Cerebral Hemmorhage)
« Last Edit: Nov 11th, 2006, 10:37pm by DL » User IP Logged

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xx Re: Alan Stanford on CROOKNECK (head/ideopathic)
« Reply #1 on: Oct 28th, 2006, 05:38am »

supplemental to the above :
http://www.nal.usda.gov/awic/pubs/Birds/vet.htm
(excerpt):
Birds that sing and die: Beta amyloid precursor protein as a marker for avian traumatic brain injury. Agnew, Dalen W.; Masliah, Eliezer; Rideout, Bruce. Proceedings of the American Association of Zoo Veterinarians Annual Conference, Minneapolis, MN. Oct. 4-10, 2003. 333 pp. p. 146-148.

NAL call no: SF605.A4

Descriptors: birds, avian traumatic brain injury, axonal injury, amyloid precursor protein marker, diagnosis

Abstract: Accurate information regarding the morbidity and mortality of zoo animals is important in their captive management and may affect the success of efforts to reproduce critically endangered species. Traumatic injury is one of the leading causes of death in avian zoological specimens and head trauma is a major subset of these cases. In veterinary patients, the ability to diagnose traumatic brain injury is often hampered by incomplete history and a lack of gross lesions or histologic evidence visible by routine staining and light microscopy. The diagnosis of traumatic brain injury is often tentative and made by exclusion of other causes. Accurate, rapid, and economic methods to document injury to the brain would provide an important tool in avian diagnostics. In the last 10 yr there has been a surge of research regarding the pathophysiology, diagnosis, and treatment of traumatic brain injury in humans. Recent advances have indicated the importance of axonal injury (AI) as a cause of morbidity and mortality. AI in humans and mammalian models can be detected with high specificity and sensitivity by immunohistochemical demonstration of â- amyloid precursor protein (â-APP). A neuronal glycoprotein, â-APP, is carried by rapid anterograde transport within the axon and accumulates in areas where that transport is impaired (i.e. sites of axonal injury). These immunohistochemical methods have been used successfully in forensics to document many kinds of mechanical injury, such as “shaken baby syndrome,”with as short a posttraumatic survival period as 30 min. To date, no published efforts have been made to apply these methods to nonmammalian species, although the presence of â-amyloid has been confirmed in an avian model and a single avian patient. The hypothesis of this study was that â-APP accumulates within the damaged axons in the brains of birds which have died from traumatic brain injury, and that this â-APP can be detected by immunohistochemical methods already developed for mammalian species. Case material was gathered from archived necropsy cases of the Zoological Society of San Diego. Sixteen adult birds were examined of which three had histologically apparent axonal lesions, and the others had either confirmed gross, histologic, clinical, or historic evidence compatible with head trauma. Two cases also had spinal cord trauma. Species included representatives from six orders (Columbiformes, Psittaciformes, Apodiformes, Passeriformes, Ciconiformes, and Gruiformes). Three birds euthanatized for unrelated reasons were used as negative controls. Human brain tissue from a patient with Alzheimer’s disease was used as a positive control. An additional 14 cases from the archives of the ZSSD in which the birds died suddenly and no diagnosis was found were also examined. Using standard immunohistochemical avidin-biotin complex techniques, two antibodies against â-APP were utilized at varying concentrations: a) â-APP (clone 22, C11; Boehringer AG, Mannheim, Germany), and b) â-APP C-terminus (CT 695; Zymed Laboratories, 561 Eccles Ave., So. San Francisco, CA 94080). The results of this study confirmed that â-APP is produced in bird neural tissue, that it does accumulate within damaged axons, and that immunohistochemical techniques developed for its detection in mammalian subjects will work in avian species. Subjectively, the use of â-APP is helpful in detecting injured axons that might otherwise be overlooked in standard H&E sections. In addition, the results of at least one case indicate that immunohistochemical staining with â-APP may detect axonal injury earlier than standard histopatholgic techniques. AI, however, was not detected in the majority of confirmed head trauma patients in this study and AI was not found in any “sudden death” cases in a population of birds which died suddenly of unknown causes. These negative results most likely reflect some of the limitations of this study, since relatively few serial sections were examined in each case and standardization of the anatomic location, post trauma to death interval, or character of the original traumatic event was not possible. The subjective increase in neuronal staining with â-APP may also be important, but these results could not be confirmed objectively without carefully matched controls. While further work utilizing cases with a well-defined trauma to death interval is needed to fully develop this diagnostic tool, â-APP immunohistochemical staining can be a potentially important new method to diagnose and study acute brain injury in avian species."

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xx Re: Alan Stanford on CROOKNECK (from injury to hea
« Reply #2 on: Oct 29th, 2006, 03:10am »

This site at link below is researching the matter of vaulted skulls (see excerpt below link)...if you would like to contribute to this research go to the site where in addition to photos they give exact instructions and address for you to contact-DL

http://www.personal.psu.edu/staff/l/a/lah161/research.html
(please go to the site link to see the first photo result of this research study)
"..........Samples Wanted:

If anyone has had the unfortunate circumstance of having one of their silkies (or any bird with a vaulted skull) die, and are curious to know if its skull has similar abnormalities, I would very much appreciate if you would send me the head. All samples would become the property of the laboratory and could not be returned to you in any way. Submitting a sample would be giving your automatic approval for me to process and photograph and/or post photos as I see fitting. I would email you set of photographs if you wish, you would just need to include a note stating this along with your email address.

Other information that would be very helpful is: age, sex and bloodline of the bird."

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xx Re: Alan Stanford on CROOKNECK (from injury to hea
« Reply #3 on: Mar 9th, 2007, 2:52pm »

in continuation of the discussion on the value of prednisone/prednisolone in cases of brain inflammation...a member reported her vet had chosen metacam(meloxicam>COX-2 NSAID) ... here is the reply after I did some research on it:

Re: [asbc] Metacam
I think that is a good idea (from what I have read in the literature) to use the metacam in this particular instance/type of inflammation (leg injury inflammation)...however...as far as its (metacam) effectivity (as compared to prednisone) in the specific instance of brain inflammation due to a peck or injury to the head/brain...well...I went back in my files and refound a few articles when I researched this when you last posted your vets choice for this drug over prednisone. I wont include here all the specific references/articles that led to my own personal conclusion that prednisone is a better choice as Alan has relayed in his treatment article (and various veterinary articles still advise) but I will include the following reference which for me was the clincher (this was in addition to other peoples usage of metacam with brain injury where,when it seemed to be ineffective and they switched to prednisone...that the pred did show an almost immediate relief of symptoms within an hour or so as compared to when they used the metacam)
....basically (in summary) this is an article looking at possible usage/effectivity of NSAID in Alzheimers Disease (referred to in the article as AD)> it is useful as it gives basic information as to the capabilites of NSAIDs to cross the brain barrier (and more specifically the specific manner of action when they do>which is entirely dependent on the specific type of NSAID> see http://www.nature.com/nrd/journal/v2/n3/abs/nrd1034_fs.html ...when researching I was specifically looking for for Cox-2 NSAID type (metacam) and its ability and effectivity in reducing brain inflammation due to injury (which is different than a neuronal disease process and the "inflammation" assoc. with it> see: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&dopt=Abstract&list_uids=12379910 ) ... now granted, the physiological differences between birds and mamals often impacts drug choice/usage (toxicity and side effect issues) however, in this instance where the basic question is > "does it cross the brain barrier sufficiently to have an anti-inflammatory effect with this specific type of injury as compared to the efficacy of prednisone" ... then one must look at the basic all round general info of the drug itself and this can be determined in general to be applicable regardless if human...mammal...avian .
Now then...specifically addressing the question as to how effective metacam (Cox-2 NSAID) is in relation to (brain injury) inflammation:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&dopt=Abstract&list_uids=11695253
".............Such agents should be devoid of COX-1-related side effects in, for example, the inhibition of blood coagulation and should only weakly affect COX-2 related functions of the central nervous system, due to slow blood-brain barrier penetration."

http://www.blackwell-synergy.com/doi/full/10.1111/j.1471-4159.2004.02743.x?prevSearch=allfield%3A%28NSAID+Meloxicam+brain%29
Classical anti-inflammatory mechanisms of NSAIDs: could they help in AD?COX and AD: the relevance of COX inhibition
The seminal observations by Vane (1971) first pointed out that NSAIDs suppress inflammation primarily through their ability to inhibit the COX enzyme. COX is the key regulatory enzyme of the eicosanoid biosynthetic pathway, which produces a variety of pro-inflammatory mediators. The inhibition of COX by NSAIDs would limit the production of pro-inflammatory eicosanoids at the site of injury. Different variants of COX have been described: COX-1, which is constitutively expressed in nearly all tissues and mainly has 'housekeeping' functions; COX-2, which is induced at injury sites by inflammatory stimuli and play a key role during inflammation; and the recently identified COX-3, whose functions are still unknown. Based on this general functional distinction, an effort was made to design drugs which selectively inhibit COX-2 and thereby are devoid of the adverse effects associated with the blockade of both COX-1 and COX-2, e.g. gastrointestinal lesions............................................Furthermore, biological data indicate that both COX-1 and COX-2 may contribute to inflammatory processes, particularly in the CNS and AD (Dubois et al. 1998; Graham and Hickey 2003; Schwab and Schluesener 2003). .......................................................These findings suggest that, once the activation of microglia is fully established, treatment with anti-inflammatory drugs would be ineffective. This hypothesis is also supported by recent evidence obtained in the same animal model with a compound combining anti-inflammatory and antioxidant properties (Wenk et al. 2004).............................Intriguingly, hippocampal neurogenesis could be restored by blocking inflammation with indomethacin (Monje et al. 2003) or with minocycline (Ekdahl et al. 2003), which is a derivative of tetracycline with anti-inflammatory properties. (see further links on this below under MINOCYCLINE)

A critical point to be considered is whether NSAIDs cross the blood–brain barrier and which drug level is achieved in the brain. The anti-pyretic effects of NSAIDs and the central side effects of certain compounds, e.g. indomethacin, suggest that NSAIDs get into the brain (Bannwarth et al. 1989). There are, however, only a few and scattered data available on the CNS levels of these drugs, possibly because they were originally developed for peripheral inflammatory diseases. In this regard, NSAIDs greatly differ for their degree of lipophilicity and, consequently, for their potential penetration into the brain with indomethacin, ibuprofen and flurbiprofen showing the highest degree of lipophilicity (Matoga et al. 1999; Pehrourcq et al. 2004). In general, brain penetration of NSAIDs is low: the levels in the CSF correspond to 1–2% of the plasma levels achieved by therapeutic doses of NSAIDs in humans and laboratory animals, for example from 0.9 to 1.5 ìm for flurbiprofen and enantiomers of ibuprofen (Bannwarth et al. 1995; Matoga et al. 1999). The kinetics of brain penetration of different NSAIDs could also influence their effectiveness in CNS chronic affections. .............................
In fact, the pharmacological characteristics of the drugs (i.e. activity on Aâ metabolism) and their blood–brain penetration properties might hamper the success of this study............"


MINOCYCLINE (a member of the tertracyline group of antibiotics)
This article also led me to a very intersting aspect being examined lately in inflammatory process:
http://www.pnas.org/cgi/content/abstract/100/23/13632
http://en.wikipedia.org/wiki/Minocycline
(wikipedia)
http://stroke.ahajournals.org/cgi/content/abstract/38/1/146
"....Lastly, minocycline significantly improved motor coordination on the rotor rod, reduced the preferential use of the unaffected limb during exploration, reduced the frequency of footfalls in the affected limb when traversing on a horizontal ladder, and improved spatial learning and memory in the water maze test.............Conclusions— Minocycline reduces functional impairment caused by cerebral focal ischemia....."


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xx misc case studies w/torticollis
« Reply #4 on: Aug 5th, 2007, 2:44pm »


TOXOPLASMOSIS
Comp Immunol Microbiol Infect Dis. 1986 ;9 (4):337-46 3802761
Avian toxoplasmosis: experimental infection of chicken and pigeon.
F Biancifiori , C Rondini , V Grelloni , T Frescura
Two groups of 13 new-laying hens each were infected by crop-route with 5000 and 50,000 infective oocysts of T. gondii. Four groups of 5 pigeons each were inoculated by crop-route with 50, 500, 1000 and 5000 infective oocysts. To each group of infected birds suitable controls were added. Hens from the experiment with 5000 infective oocysts were apparently resistant to the infection and they had no clinical signs in the succeeding 40 days p.i. Hens from the experiment with 50,000 infective oocysts showed an egg-drop and mortality in embryonated eggs, especially during the first 2 weeks p.i. Isolation of the parasite was unsuccessfully attempted from 720 embryonated eggs, produced by infected groups, and tested on various days p.i. and at different stages of infection. The parasite was isolated from the brain, heart, liver, spleen and lung of infected birds 7 and 15 days p.i.; 40 days p.i. it was evident only in brain and heart. IgG onset and mean course were monitored by ELISA and high titers were reached by both groups. Pigeons from groups 500, 1000 and 5000 developed rapidly progressive clinical signs as diarrhea, trembling, incoordination, torticollis and death. They had enlargement of liver and spleen and focal necrosis, nodular features in the crop. Pigeons from expt 50 had no clinical signs in spite of the presence of the parasite in their organs for over 45 days p.i. Parasite was isolated from brain, heart, liver, spleen, lung, kidney, crop and muscles from all infected groups. Histopathological and ultrastructural features revealed the presence of multiplying tachizoites even within cells of the crop. Seroconversion, as monitored by ELISA, was recorded in all infected groups although high ELISA-titres were never reached. One of the negative controls from expt 5000 developed specific antibodies but the parasite was not isolated from its organs.

LISTERIOSIS:
Avian Dis. ;47 (4):1496-502 14709003
Pathology of listerial encephalitis in chickens in Japan.
Mitsuteru Kurazono , Kikuyasu Nakamura , Manabu Yamada , Toshirou Yonemaru , Toyoaki Sakoda
Neural signs (torticollis, drowsiness) and mortality were observed in five chickens of a native chicken flock (reared for meat) that included 450 male birds on a farm that had 2300 native chickens and 1120 layers. Histologic lesions were observed in the medulla oblongata, optic lobe, cerebellum, and spinal cord of the affected birds. The lesions, which were most severe in the medulla oblongata, were massive abscesses with rarefaction (demyelination and malacia) of the parenchyma with gram-positive bacteria. The degenerative and necrotic areas were characterized by fibrin thrombosis, hemorrhages, and congestion in the blood vessels. Immunohistochemically, the bacteria positive for L. monocytogenes antigen were observed in the medulla oblongata, cerebellum, and spinal cord. Ultrastructurally, the small rod-shaped and thin-cell-walled bacteria were observed in the parenchyma of the medulla oblongata. Listeria monocytogenes (serotype 4b) was isolated from the medulla oblongata and spinal cord. The pathogenesis of listerial encephalitis in chickens was discussed.

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