Dragonflies and Dandelions
Practical Matters >> EMERGENCIES >> CROOK/WRY NECK / LIMBER NECK/TORTICOLLIS
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CROOK/WRY NECK / LIMBER NECK/TORTICOLLIS
Post by DL on Oct 15th, 2006, 11:10am

Twisted/Crookneck...Limberneck...Stargazing...Torticollis ...these terms are interchangeably used to describe a neurologically induced symptom involving the neck which is involved in many conditions and imbalance (ataxia) is usually often also involved (see first link below which gives a good overview of the different diseases and conditions associated with it)... age and breed often gives a clue to narrowing down what the cause is and even though leg paralysis may indicate Mareks it is by far not the only condition >>>brain/head injury or toxic challenge is far more common when leg paralysis suddenly occurs and there are several nutritional deficiencies as well as heavy metal/lead toxicity (which is often not considered with poultry) as a possible cause.
(see the DISEASE category for MAREKS and Toxicoses/Plant toxicities etc. and the NUTRITION category for nutritional deficiencies in addition to the overview given in the link below)-DL


http://www.petplace.com/birds/ataxia/page2.aspx
An EXCELLENT article discussing the various causes of ATAXIA in birds
(excerpt)
"...Ataxia may be defined as an inability to coordinate the voluntary movement of muscles. Birds that are ataxic appear wobbly or clumsy and will often stand with the legs spread far apart in order to balance or hook their beak on the side of the cage. When severely ataxic, they will stumble and fall ..."

CROOKNECK DUE TO HEAD INJURY (particularly with Silkies and crested breeds such as Polish)>>>see the following CASE STUDY thread which includes Alan Stanfords excellent treatment article:
http://dlhunicorn.conforums.com/index.cgi?board=casestudiesemergencies&action=display&num=1160927052

http://www.cliniciansbrief.com/cms/portals/_default/pdfs/capsules/Aug_05_Cap14.pdf
Steroids in Neurological Disease: When and Why?

http://www.pjbs.org/ijps/fin714.pdf
Vitamin Deficiency-Induced Neurological Diseases of Poultry
(excerpt)
Broad signs of
-vitamin A deficiency in the nervous system include
ataxia, constricted optic nerve and increased
cerebrospinal fluid ...

Thiamin (B1): This vitamin deficiency -in animals- is in chickens are inflammation of the upper
characterized by appetite and weight loss, cardiac and
neurologic symptoms. The latter, particularly in birds, is
seen as a severe hyperextension and spastic tendency
in which the individual enters a complete ‘bridging’ or
‘arching’ position with the head, neck and spinal column
arching backward in extreme extension, most commonly
known in the field as stargazing
...."

http://www.ivis.org/advances/Kearns/kearns2/ivis.pdf
(ASPERGILLOSIS)
"...Focal Granulomas - Focal granulomas in the brain can occur in any species, but they are most often seen in waterfowl, especially eider ducks. Central nervous system signs such as ataxia or torticollis may be
present. As with the syringeal granuloma presentation, the lower respiratory tract may simultaneously be
affected, or the CNS granuloma may occur as a single lesion. Focal granulomas may also occur outside the CNS, causing signs such as unilateral paresis or unilateral pectoral muscle atrophy...."

http://www.parrots-at-play.org/aspergillosis.htm
another EXCELLENT article on aspergillosis

http://www.asasea.com/pd-sect1.html
(excerpt)
"The differential diagnosis of ataxia includes avitaminosis A, avian encephalomyelitis (epidemic tremor), thiamine and pyridoxine deficiencies. Recently, arenavirus infection has emerged which leads to hypoglycemia shown as recumbency and tremors. Organophosphate toxicity which causes incoordination and death preceded by convulsions is usually rapid in onset and involves the entire flock.......................

Encephalomalacia occurs in chicks fed diets in which vitamin E has been destroyed by oxidative rancidity. The presence of free radicals will result in destruction of vitamin E both in the feed and in vivo. ..........................
The effect of avitaminosis E is exacerbated by concurrent deficiency in sulphur-containing amino acids and selenium.................Encephalomalacia is the most commonly encountered condition associated with avitaminosis E .........Infected birds demonstrate ataxia, incoordination, and terminal recumbency with cycling motions of the legs.......

Vitamin B1 (Thiamine) Deficiency
This condition occurs as a result of failure to add thiamine to vitamin premixes or occasionally as a result of excessive addition of the anticoccidial, amprolium, to diets. The principal sign of thiamine deficiency in 10 to 20 day old chicks comprises incoordination and an abnormal retraction of the head ("star gazing"). ..........."

http://www.iffco.nic.in/applications/animalinfo.nsf/2e53b634b399e0d965256a1800339557/14658564226b21a265256a1e0042f163?OpenDocument
..."ii) Manganese deficiency :
Causes low lhatchability, chondro dystrophy, thick legs, short wings, parrot beak, globular head and PEROSIS. In chicks ataxia is produced when excited ...Head is drawn forward and bend underneath or retracted over back.....
..............Aflatoxin can be produced in the crops while growing in the field and also during harvesting, storage, processing/ mixing, transportation seed/grains as well as during the period of feeding. The production of aflatoxin is rapid when the moisture content is more than 15%, temperature is about 24o and relative humidity is more than 80%. Kacha and damp floor as well as improper ventilation favour the production of aflatoxin.
The main symptoms produced are lethargy, listlessness, loss of appetite, decreased feed efficiency, closing of eyes, opisthotonus, spasm of the neckmuscles, arched back and legs stretched posteriorly. There is retardation of growth in growing birds and drop in egg production in layers. The hatchability is also poor. The birds become more lsusceptible to other infections and there is immunity breakdown....."

http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/71719.htm
(Botulism as cause of crook neck)
MERCK Veterinary Manual
..."These fly larvae have also been associated with toxic effects in chickens. Botulism (see Botulism: Introduction), also known as limberneck in chickens, has been associated with ingestion of large numbers of larvae of Lucilia caesar , Phaenicia sericata , and other species of flies. Clostridium botulinum multiplies in carrion, where it may be picked up by fly larvae breeding in that medium and then passed on to chickens that eat the maggots..."

http://www.birdsnways.com/wisdom/ww72eiv.htm
Another possible cause of loss of balance is an ear infection:
(excerpt)
"Otitis externa is an inflammation of the external ear. It may by caused by bacterial or fungal organisms. Pruitis or itching may be present, causing the bird to scratch his ear or rub his head on the perch. The ear opening may be swollen and red and the feathers may be matted with a discharge.

Viral diseases such as paramyxo virus can cause otitis interna, resulting in loss of balance and torticollis (abnormal twisted head position - head turned upside down.) "

REOVIRUS and neurological symptoms:
http://www.thepoultrysite.com/articles/96/avian-reovirus-infections
(Reovirus/Malabsorption can be the underlying cause of neurological symptoms incl. crookneck)
http://www.pjbs.org/ijps/fin696.pdf
International Journal of Poultry Science (2006)
Selenium Sources Affect Protein Concentration....(full text) > small excerpt from abstract findings:
...""our findings suggest that ARV (avian reovirus) infection depresses growth, increases mortality and reduces protein concentration in various tissues, whereas SE is beneficial against ARV infection in broilers through an improved antioxidant status..."

http://www.spc.int/rahs/Manual/AVIAN/AVENCEPHALITISE.htm
(excerpt)
".... Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors). ...................

Clinical signs
Chickens of all ages are susceptible, but clinical signs of encephalitis only develop in those younger than four weeks. The disease is similar in turkeys and chickens. Under field conditions disease is most common in the 1–2 week age group. Following initial dull expression of the eyes, the following signs are seen:
- progressive ataxia with the chick losing control of legs, sitting on its haunches and falling onto its side;

- tremor of the head and neck.

Ataxia progresses to paralysis and death results from inability to feed or drink, or through being trampled.

Some birds recover, and others may survive with persistent clinical signs.

In susceptible adult birds, infection is usually sub-clinical, although there may be a transient drop in egg production...................

Differential diagnosis
Newcastle disease
St Louis encephalitis
ricketsiosis
vitamin E deficiency
vitamin A deficiency
riboflavin deficiency
perosis

Specimens required for diagnosis
Samples of brain tissue should be collected for histopathology, fluorescent antibody testing and/or virus isolation.
Serum sample from young chicks should be collected for ELISA test.

Transmission
AE virus is transmitted both vertically and horizontally i.e. through the egg and by contact. Eggs laid by hens with sub-clinical infection will carry the virus. While hatchability drops, eggs will hatch and chicks will develop clinical disease soon after. Affected chicks shed virus in faeces and will infect susceptible in-contact chicks.
To date wild birds have not been incriminated as reservoirs.

Risk of introduction
AE could be introduced through the import of sub-clinically infected adult breeding stock, infected day-old chicks or hatching eggs..................."













Resulting from ear disease
Post by DL on Aug 8th, 2007, 7:35pm

VESTIBULAR Disease and nuerological symptoms:
http://neuro.vetmed.ufl.edu/neuro/vestibular/vestib.htm
(A technical article on Vestibular Disease (veterinary) and not bird specific)
(small excerpts)
...."Partially due to this concern, vestibular diseases represent a large number of neurologic referrals. Often, it is only reassurance that the problem will pass that is necessary. Recognition of when to intervene is as important as when not too.

The cardinal signs of unilateral vestibular disease are head tilt, nystagmus (spontaneous abnormal eye movements), circling (toward the lesion in "tight" circles), and incoordination. This is because the vestibular system is an important part of the CNS balance control system. In order for animals to know how they are oriented in space, three neural systems must be functioning. The vestibular system, through the stimulus-response of the hair cells in the semicircular canals, reacts to angular acceleration and deceleration. The visual system allows the animal to focus on the horizontal and vertical, orienting in space. Finally, gravity is detected by pressure receptors in the skin, orienting the animal on up and down. While the vestibular system is very important, it requires at least 2 of these orienting systems to function for the animal to negotiate within its environment. This can be important with vestibular disease, since, in acute disease, the nystagmus prevents the eyes from focusing on the horizon, effectively eliminating spacial orientation..............
Vestibular diseases can be classified into three major disease processes: idiopathic vestibular disease, inner ear disease, or central vestibular disease. The former 2 represent common forms of peripheral vestibular disease which need to be separated from each other and from central vestibular disease..............

The diagnosis of idiopathic vestibular disease is tentatively made by the presence of acute clinical signs in the absence of other physical findings... It is most likely that idiopathic vestibular disease is an immune-related condition affecting the unique antigens presented by the vestibular nerve. It can recur and is often more severe on recurrence..............

Inner Ear Disease:
Many different problems result in inner ear disease; however, the clinical signs caused by these diseases are similar, indicating the location of the disease rather than the specific cause. These signs are those of peripheral vestibular dysfunction, including head tilt, nystagmus, circling and imbalance. On the other hand, since the diseases which cause inner ear disease are usually slower in evolution, these signs are generally less severe than with idiopathic vestibular disease.......The most common cause of inner ear disease in all species is secondary in inner ear infection. Most of these represent bacterial extension from otitis media which can arise from hematogenous spread from bacteremia or from spread up the eustachian tube to the middle ear. Luckily, these infections, once recognized, can often be successfully treated. Other causes of inner ear disease may not be treatable, including fungal infections and neoplasia. Therefore, it is generally best to "treat-for-the-treatable" when dealing with inner ear disease, using appropriate antibiotic therapy. ........
The treatment of bacterial inner ear infection must consider the fact that the disease represents bone infection. As such, the antibiotic must be able to penetrate bone, develop good tissue concentrations (including the blood-ear barrier) and, preferably, be bactericidal in action. Many veterinarians use enrofloxacin as their antibiotic of choice. I find that enrofloxacin is great for treating gram negative infections in the lung, but it may not reach tissue concentrations within neural structures like the inner ear. It needs additional help to do this. Therefore, if I do not use my treatment of choice, I will add a sulfa drug to enrofloxacin to take advantage of the synergistic effect of sulfa drugs. My antibiotic regime of choice is cephalosporins and sulfa drugs (sulfadimethozine) in combination. This meets the criteria for the ideal therapy for inner ear disease. It is excellent in treating gram positive bacteria, which are the most common organisms infecting the inner ear......

Central Vestibular Disease:
Whenever anything else is seen other than the signs above, one must consider the likelihood that the problem is due to central vestibular disease. Additional cranial nerve deficits, proprioceptive deficits and motor deficits indicate brainstem damage affecting the vestibular nuclei and sensor and motor pathways which course through the vestibular region of the brainstem. In addition, the nystagmus seen in central vestibular disease will often be vertical or positional in nature, supporting the location of the disease process within the brainstem or cerebellum. If there is whole body and head tremors, the lesion is likely to be within the flocculonodular lobe of the cerebellum. While diseases which affect the peripheral vestibular system are usually good diseases; that is, diseases which regress without treatment or which respond to appropriate antibiotic therapy, most central vestibular diseases carry a less optimistic prognosis.

The major causes of central vestibular disease are inflammatory/infectious diseases or neoplasia. Organophosphate intoxication, liver disease (with metabolic brainstem degeneration) and thiamine deficiency can occasionally result in central vestibular disease (depending upon the species of animal), but these causes are far less than the inflammatory or neoplastic causes...............who are not eating and stressed can easily develop thiamine deficiency and this should not be overlooked in treating ....................
So, while central vestibular disease has many causes, in the absence of specific disease processes, there is limited hope for successful treatment and that hope is often based upon the response of the animal to medical management. The medical management is largely based upon the responsiveness of the disease process to corticosteroids. In other words, there are many causes of central vestibular disease, but often only one treatment approach. If the client understands this, it is possible to treat central vestibular disease without a specific diagnosis, realizing that the response to therapy can suggest whether the disease was "good" or "bad". The treatment approach that I use when a specific diagnosis cannot be made (either because the patient is too ill to undergo the diagnostic test or the client cannot afford them) is to treat with corticosteroids (usually oral prednisolone) and antibiotics (doxycycline and sulfadimethozine). The prednisolone will reduce inflammation while the doxycycline can help control bacterial and rickettsial disease while the sulfadimethozine may help control protozoal infection. .........since toxoplasmosis and cryptococcosis might be treatable......also add parenteral thiamine therapy when treating .........


http://www.vetpathology.org/cgi/content/full/39/3/396
Ataxia and Disequilibrium in Domestic Ducks (Anas platyrhynchos f. dom.) with Intracranial Lipomas
(excerpt)
"....Intracranial fat bodies occur in 82.3% of domestic ducks with feather crests.1 The gross and histologic appearance of these intracranial fat bodies is similar to that of intracranial lipomas reported in humans and other mammals.5,6,12,14 Paradoxically, intracranial lipomas are often clinically silent in affected ducks, possibly because the skull is pliable until cranial bone fusion.2,4 Increased cranial volume may delay or avoid increased intracranial pressure by neurocranial enlargement and may account for the rare occurrence of central nervous system clinical signs in spite of the high incidence of intracranial lipomas in this breed of ducks.1 However, lipoma-induced central nervous clinical signs can appear previous to suture closure in humans and other animals.5,6,10,11,13 More subtle neurologic defects may be present in morphologically abnormal Crested ducks.

Intracranial lipomas are usually regarded as congenital malformations and may result from abnormal differentiation of the meninx primitiva, the mesenchymal anlage of the meninges.5,6,13,14 Localization of these lipomas to the tentorium cerebelli in Crested ducks agrees with this hypothesis. The high incidence of intracranial lipomas in Crested ducks points to either a linkage between their formation and that of feather crests or to pleiotropic effects of the gene for crests...."



Resulting from LISTERIOSIS
Post by DL on Jan 26th, 2010, 4:10pm

On occasion, LISTERIOSIS can become pathogenic and cause the symptom. PLEASE BE AWARE IF YOU ARE PREGNANT and your bird displays this symptom , that even though it rarely occurs, that Listeriosis can be very dangerous (the following article in the MERCK veterinary manual on the disease in poultry gives details and warning:
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/203200.htm
role of amprolium/thiamin(B!) deficiency
Post by DL on Nov 29th, 2010, 02:42am

It is important to give a B vitamin supplement to birds exhibiting neurological symptoms (wryneck/stargazing or leg/balance problems) as the links/studies below support. Some are concerning Amprolium as this interferes with thiamin (adult stock given amprolium with no vit supplement after can lead to chicks with thimamine deficiency) This is also why after cocci treatment with amprolium a (general)vit/nutritional supplement incl extra attention to the B vitamins is advised (AviaCharge 2000 with polyvisol for instance)
photo of thiamine dfeficient chick
http://www.ncsu.edu/project/swine_extension/nutrition/nutritionslides/27.jpg

http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/206934.htm
MERCK manual page on thiamin deficiency (note its warning on impaired nutritional/vitamin uptake)

http://jn.nutrition.org/content/76/1/59.full.pdf
excerpt: "....These authors showed that the composition of the diet can influence thiamine
levels in yolk, indicated that chicks
from hens fed diets low in thiamine die
from polyneuritis soon after hatch,...."

http://aem.asm.org/cgi/reprint/16/6/961.pdf
(on amprolium)