Tina Neuro Papers Flashcards
1
Q
3 manifestations of ataxia
A
: vestibular, cerebellar and general
2
Q
Ipsilateral facial neuropathy accompanies most cases of PVD due to
A
its close approximation to the vestibular nerve within the internal acoustic meatus and petrosal portion of the temporal bone.
3
Q
most common clinical presentations of unilateral PVD and facial neuropathy in the mature horse
A
Temporohyoid osteoarthropathy
4
Q
Important differentiating observations of central vestibular dysfunction compared to peripheral dysfunction are…
A
mentation changes,
presence of other cranial nerve deficits (facial nerve exception),
postural reaction deficits or UMN paresis.
5
Q
which horses tend to show Cerebellar ataxia
A
much more common in the neonate and foal.
may be developmental, as in cases of cerebellar abiotrophy and Dandy-Walker syndrome,
unusual in the mature horse: acquired from structural or inflammatory disturbances in the mature horse
6
Q
Clinical observations in cerebellar ataxia
A
- distinct hypermetria of the thoracic and occasionally pelvic limbs, which may worsen with gait speed.
- Postural reaction tests may be normal to exaggerated.
- Intention tremors of the head may be observed during voluntary movement or when stationary due to disturbances of cerebellar influence on fine motor control.
- Absent menace response may be observed with loss of cerebellar integration of the evoked blink reflex.
- Appropriate mentation is commonly observed in cases of congenital cerebellar disease but not aquired disease
7
Q
General proprioceptive ataxia can occur with any injury affecting
A
the sensory (afferent) components of the central nervous system; however, most spinal cord injuries disturb both sensory and motor (efferent) components given their anatomic proximity.
8
Q
where are the lumbosacral intumescences
A
(L4–S2)
9
Q
Extremely low head carriage, absent evidence of trauma, is suggestive of
A
a central nervous system or neuromuscular disorder.
10
Q
explain the cutaneous trunci reflex
A
can be triggered by tapping a blunt instrument along the dorsolateral dermis from the tuber coxae cranial to the shoulder.
Afferent stimulus is carried via spinal nerves to spinal cord motor neurons cranial to the
C7–T1 segments
and the efferent response is carried via the lateral thoracic nerve to the cutaneous trunci muscle
11
Q
Regional loss of the cutaneus trunci reflex is inidicative of
A
thoracic SCD or
brachial plexus/lateral thoracic nerve injury.
12
Q
What to do when the horse is severly lame during a neurologic exam ?
A
Re-examination is advised following regional or intra-articular anaesthesia.
13
Q
The appearance of a pacing gait in non-characteristic breeds suggest
A
ataxia
14
Q
Toe-dragging while backing is a compensatory sign of
A
weakness and decreased proprioception without the ability to visually compensate for limb placement
15
Q
Which benefits does the Raising of the head while walking have during neurologic examination?
A
removes visual compensation of thoracic limb placing and alters vestibular/proprioceptive influence on gait, increasing the dependence on proprioception and motor integration.
Mild thoracic limb hypermetria and delayed cranial phase of stride is expected in clinically normal horses while walking with the head raised, described as floating.
16
Q
Spinal cord dysfunction of the cervical spinal cord segments (C1–C5) results in
A
- UMN tetraparesis and general proprioceptive ataxia in all limbs. The severity of ataxia may appear more severe in the pelvic limbs and subtle in the thoracic limbs.
- +/- Horner
17
Q
Caudal cervical SCD (C5–T2 segments) can result in
A
- LMN dysfunction of the thoracic limbs and
- UMN dysfunction of the pelvic limbs.
18
Q
Thoracolumbar spinal cord segments T3–L3 SCD results in
A
- UMN paraparesis and pelvic limb general proprioceptive ataxia.
Compared with cervical SCD, thoracolumbar dysfunction is less common, or infrequently recognised in the horse.
19
Q
Defining features separating UMN from LMN paresis localisation in the ambulatory horse include:
A
- presence of ataxia (LMN dysfunction is not associated with ataxia),
- absence of the cutaneous trunci reflex (bilaterally suggests UMN pathology of C8–L3 spinal cord segments or associated spinal nerves) and
- intact extensor postural reactions (ability to support weight on the limb).
- Patellar hyperreflexia may be present in recumbent horses.
20
Q
The lumbosacral intumesence and terminal spinal cord (conus medullaris) are located within
A
Lumbosacral spinal cord segments L4–S2
- Thus SCDs cranial to the L4 vertebra cause general proprioceptive ataxia and UMN tetra/paraparesis.
- Injuries caudal to the L4 vertebra result in LMN deficits from dysfunction of the neuron cell bodies (spinal cord) or spinal nerves.
21
Q
Polyneuritis equi (cauda equina neuritis) affects
A
the spinal nerves of the lumbosacral and coccygeal segments causing LMN deficits recognised as
- loss of cutaneous sensation,
- loss of perineal reflex,
- weak tail/anal tone and
- urinary incontinence.
22
Q
most common deficits in horses with temporohyoid osteoarthropathy
A
The most common signs included
- auditory loss (100% of horses),
- vestibular and facial nerve dysfunction (83%), and
- exposure ulcerative keratitis (71%).
- Concurrent left laryngeal hemiparesis was observed in 61% of horses through endoscopy.
23
Q
unilateral or bilateral auditory dysfunction on THO?
A
Auditory dysfunction was bilateral in 50% of the cases (complete and partial), and unilateral affecting more commonly the right ear
24
Q
THO is
A
disorder of temporohyoid joint formed by the stylohyoid and petrous temporal bones.
The disorder is characterized by bony proliferation, fusion of the joint, and potential fracture of the involved or adjacent bones
25
etiology THO
Proposed etiologies include
* inflammation,
* infection of the middle/ inner ear secondary to a hematogenous or ascending infection from the upper respiratory tract,
* extension of external ear infection, and
* primary degenerative process.
26
Clinical signs of THO
Clinical signs vary
* **head shaking,**
* apparent r**esentment of manipulation of the head or ears**,
* **resistance to the bit,**
* **difficulty eating**, and
* **facial and vestibulocochlear nerve dysfunction.** (Auditory loss appears to be a common neurologic abnormality in these horses)
27
Prognosis of auditory loss in THO
Despite observed overall neurologic improvement (facial and vestibular function) in diseased horses, **auditory dysfunction persisted** (clinical evaluation: short-term n = 19/19, long-term n = 16/ 16; BAER evaluation: long-term n = 8/8). **Further, auditory loss progressed in 3 of 5 horses with bilateral disease.** However, this deficit did not appear to interfere with the horses’ daily activities
28
The carrier status of lavender foal syndrome (LFS), cerebellar abiotrophy (CA), severe combined immunodeficiency (SCID), and occipitoatlantoaxial malformation (OAAM1) in foals with juvenile idiopathic epilepsy (JIE)?
Ten Egyptian Arabian horses (5 females and 5 males) were phenotyped as foals with JIE by electroencephalography (EEG).
**All foals were negative for the genetic mutations** that cause LFS, CA, SCID, and OAAM1 except for 1 foal that was a carrier of CA.
29
Juvenile idiopathic epilepsy
(JIE) is a self-limiting epileptic syndrome described in Egyptian Arabian foals.1 This disorder is characterized by recurrent generalized tonic-clonic seizures with no apparent precipitating events or underlying disease with an early onset in life (median age, 2 months).1 Affected foals are clinically normal between seizures.1
30
Neuroglycopenia refers to
a shortage of glucose in the brain resulting in neuronal dysfunction and death if left untreated.
Neuroglycopenia is presumed to occur in horses as the **result of severe hypoglycemia**. Subclinical seizures, and intermittent blindness and deafness of cortical origin can occur. Severe altered state of consciousness and seizures can be observed at a blood glucose cut-off value of \< 42 mg/dL
31
Sidewinder gait in horses
characterized by walking with the trunk and pelvic limbs drifting to 1 side.
Can be of neurological/orthopedic/muscular origin
The condition often has a poor prognosis for function and life
Case fatality was 79%.
32
central nervous side affects of gentamicin in horses
Aleman 2021: Seven out of ten horses had auditory loss after 7 day course of Genta:
complete bilateral (N = 1),
complete unilateral (N = 2), and
partial unilateral ((N = 4)
long term???
33
In vitro differntiation of different nerve fibers and findings in the recurrent laryngeal and phrenic nerves
**Immunohistochemistry of FFPE-derived nerve samples with selected antibodies** and specific antigen retrieval methods, enabled **identification of myelinated and unmyelinated axons, cholinergic, sympathetic and peptidergic axons**.
The recurrent laryngeal and phrenic nerves are composed of
* **myelinated cholinergic (motor),**
* **myelinated sensory** fibres and **unmyelinated peptidergic (sensory)** axons.
* **unmyelinated adrenergic** (sympathetic) axons
34
Shivering is...
Equine shivering is a **neuromuscular disease with characteristic signs of intermittent muscle fasciculations or ‘shivering’ of the hindlimb muscles** that is elicited by specific locomotor movements [1,2].
Walking backward often results in either a hyperflexed abducted hindlimb or a rigidly extended hindlimb, whereas forward gaits often appear normal [3].
Hindlimb hyperflexion in horses with advanced shivering, however, can occur with initiation of forward walking or directional changes [3,4].
35
new conclusions on 2018 shivering study
In summary, our data provide the first **electrophysiological evidence** that equine shivering is **characterised by enhanced simultaneous recruitment of flexor and extensor muscles** and a **loss of the ability to modulate motor unit recruitment in the hindlimbs**, particularly when walking backward.
Abnormal muscle activation in horses with shivering was consistent with the observed hyperflexion or hyperextension of hindlimbs and was **associated with the presence of selective Purkinje cell axonal degeneration in deep cerebellar nuclei.**
36
Reported prevalance of CVM in Thoroughbred horses
1.3–2%
37
Evidence based conservative treatment for adult horses in Cervical Vertebral Stenotic Myelopathy, indications and outcomes
Indication:
Horses with
* **milder grades of ataxia (less than grade 3)**,
* **normal vertebral canal Minimal Sagital Diameter ratios** and
* **moderate Articular Process Joint changes (grade 3a–4b)**
are good candidates for medication (Hepburn 2012).
**intra-articular medication**
* corticosteroids: _32% of horses improved performance_ although in _50% of the improved cases the effect lasted only 1–6 months_
* **Older ataxic horses had a 60% improvement** with an average **2 grades improvement** of ataxia that was effective for **1–8 years (average 2 years)** (Kristoffersen et al. 2014).
38
Causes and sites of CVSM in the sceletally mature horse
In the skeletally mature horse, clinical signs of CVSM are due to **degenerative pathology of the articular process joints and the surrounding soft tissues** that result in _static (most commonly)_ or _dynamic_ cord compression most commonly in the **caudal cervical articular process joints (C5 to T1)**
39
Ttrm of CVM in the young horse
What is the evidence?
Conservative treatment consists of combinations of
* strict stall confinement,
* anti-inflammatories and
* dietary modifications designed to reduce growth spurts in younger horses.
**Resolution of neurological signs was observed in 75% of mildly affected (neurological) foals or yearlings** with equivocal radiographic changes who were **fed decreased protein and low nonstructural carbohydrates** (total 1.5% bodyweight, which is 75% of the 2% bodyweight recommended feed for normal horses) with soaked hay, **vitamin E and selenium** and had **prolonged total confinement** (Donawick et al. 1993; Kronfeld 1993).
40
evidence on surgical correction of CVM
**favourable long-term outcome in yearlings and skeletally mature horses for resolution of ataxia.**
Although success rates of surgical correction in horses up to 18 months of age in which the dynamic form of CVSM are more commonly seen are greater (improvement 1-2 ataxia grades over 2 years), good outcome for mature horses with static degenerative myelopathy are also reported.
41
APJ OC in foals and its link to CVM
Articular process joint OC in Warmblood foals is common and is **not more prevalent** at CVM predilection sites, suggesting that abnormalities of enchondral ossification _may not be major contributors to CVM_.
42
most common cause of facial nerve paralysis
Sixty-four equids
* **trauma (n = 20)**
* central nervous system (CNS) disease (n = 16),
* idiopathic (n = 12): 4 “true” idiopathic, 8 “not investigated”),
* temporohyoid osteoarthropathy (n = 10),
* otitis media-interna (n = 3),
* lymphoma (n = 1),
* iatrogenic as a consequence of infiltration of local anesthetic (n = 1), and clostridial myositis
Facial nerve paralysis was unilateral in 92% (59/64) of cases and bilateral in 8% (5/64) of cases.
43
long term follow up of facial nerve paralysis
**Twenty-nine (53%) equids had full resolution of FNP,**
14 (25%) were euthanized,
6 (11%) partially improved, and
6 (11%) were unchanged or worse.
44
probably most common type of postanesthetic facial nerve paralysis
when the head of the anesthetized horse is positioned in such a way that the _halter or other firm object compresses_ the **buccal branches** of the nerve as they _cross the masseter muscle._
causing **lip droop or muzzle deviation** alone.
45
Most common cause of FNP in humans and evidence based ttrm
In human medicine, **idiopathic FNP (Bell's palsy)** accounts for approximately **70% of cases of FNP.**
In 2007, a double-blinded, placebocontrolled, randomized study with 551 participants reported **significant improvement** in patients treated **with prednisolone within 72 hours of onset**. In small animals, the benefit of corticosteroid administration is not known.
46
signs of facial nerve paralysis and how often do they occur
* 69% **deviation of the muzzle**
* 63% **drooping of the lip**.
* 55% **ear droop or bilateral ear droop**
* 53% **Inability to blink the eye** on the affected side
* 52 % **ptosis of the eye**
* * 53% of cases had ≥3 signs of FNP, and
* 16% of cases had all 5 signs (ptosis, ear droop, muzzle deviation, absent blink, and lip droop).
* Additional signs attributed to FNP included nares collapse (3 cases, in 1 case bilateral, causing respiratory distress).
47
Kennedy et al. (2016) assessed the oral microbiome of horses with and without periodontal disease and found that
affected horses had a different, more diverse microbiome, with Prevotella species being the most prevalent.
48
Congenital occipitoatlantoaxial malformation in Warmbloods
1 case report in 3 yr old WB mare including not only bony but muscular malformation
mostly arabian foals affected
Most horses affected by OAAM _develop ataxia due to compressive damage to the spinal cord secondary to the bony malformations early in life_.
Imostly in foals (Mayhew et al. 1978a; Gonda et al. 2001).
In some cases, ataxia develops progressively to the age of 2–3 years (Wilson et al. 1985).
no trtm, mostly euthanasia
49
comparison between
percutaneous, ultrasound-guided CSF collection from the C1-C2 space in standing horses
Lumbosacral (LS) centesis in standing horses
CSF from C1-C2 space: **decreased likelihood of clinically important blood contamination of samples.** (significantly lower mean protein concentration and red blood cell count)
* Collection time,
* total nucleated cell count,
* EPM titers, and
* serum:CSF EPM titer ratios
were not significantly different between collection sites
50
Does repeated CSF collection alter CSF analytes?
Repeat thecal puncture from the LS or C1-C2 space 2 weeks apart does not appear to impact CSF analytes.
51
Are dysphagic foals less likely to race as adults and have altered athleticism (age of first race, Speed Index, Earnings Per Start Index) compared to healthy foals that raced as adults.
No. The athleticism of formerly dysphagic foals does not appear to be negatively impacted compared to normal foals as measured by age of first race, Earnings Per Start Index and Speed Index.
52
Electroacupuncture in headshaking
report with 6 horses with grade 3 headshaking:
all responded ACCORDING to the OWNERS
electroacupuncture of the **infraorbital nerve** under light sedation. The nerve was _stimulated with alternating 2 and 80 Hz frequencies for a period of 25 min_ with the current adjusted so that there was v_isible twitching of the nostrils and/or lips_.
Follow-up treatments were given when the signs recurred or 4–7 days later if there was no initial response. Once a response was achieved, the period of remission often increased with subsequent treatments.
53
Osteochondroma of the cervical spine
imaging
Osteochondroma of the cervical spine is an uncommon benign neoplasia of the cervical spine with clinical symptoms related to its location with respect to adjacent structures.
CT guided biopsies.
54
Spondylosis deformans in horses
clinical signs, diagnosis, ttrm, prognosis
low head carriage or difficulty lowering head or flexing
diagnosed w/ lateral radiographs
Spondylosis deformans (VENTRAL)is rare, typically identified from **T10–T14** and, rarely, the lumbar spine in horses. largest lateral motion and axial rotation of the equine spine -\> spondylosis?
Prognosis guarded, conservative ttrm with NSAIDs possible
55
cervical and cranial thoracic Discospondylitis
= inflammatory condition involving the vertebral bodies adjacent to the intervertebral symphysis and their associated intervertebral disc.
**unusual in horses** and the majority of documented cases have been associated with infection.
This study 2020: 8 cases presumably non infectious
clinic:
* neck stiffness,
* neck pain,
* a stiff or shortstepping forelimb gait and forelimb lameness.
* Ataxia is also reported as a clinical sign, associated with protrusion of disc material into the vertebral canal
dx: intervertebral disc space obliteration in lateral radiographs
ttrm: surgical fusion of the affected joints
56
Phosphorylated neurofilament heavy protein (pNfH) as a serum biomarker
for detection of axonal degeneration
Serum pNfH concentrations are specifically increased (\>1 ng/mL) in some horses with
* equine neuroaxonal dystrophy and the more severe pathological variant,
* equine degenerative myeloencephalopathy.
* _99% specificity and 12% sensitivity_
Increased CSF pNfH concentrations (\>3 ng/mL) can be observed with eNAD/EDM or CVCM.
in other studies Serum pNfH concentrations were significantly higher in EPM-affected horses compared to control horses and CVCM-affected horses, whereas
CSF pNfH concentrations of EPM-affected horses were reported to be four times higher than CVCM horses in this study and far higher in another one
therefore, it is **unlikely that the magnitude of increase can be associated with a particular disease entity**
57
pastureassociated stringhalt (PSH)
what is it
causes
clinical signs
risk factors
diagnosis
treatment
prognosis
= peripheral neuropathy affecting the larger myelinated axons
cause: thought to be the result of exposure to a plant-derived neurotoxin, precise aetiology unknown
clinic: **exaggerated, prolonged hindlimb flexion -** exacerbated when affected horses appear agitated or disturbed.
risk factors:
* Drought-affected, poor-quality pasture
* presence of Hypochoeris radicata (löwenzahn)
* mature and taller animals
Dx of stringhalt has to be based on the clinical signs and absence of other neurologic and orthopaedic abnormalities.
ttrm: experimental
prognosis: Most horses recover spontaneously if removed from the presumptive source of toxin; recovery can be prolonged (years) and incomplete in occasional cases.
58
Peripheral neuropathy of a forelimb in horses: 27 cases
predominant lesions
prognosis
Predominant lesions:
* radial nerve 14 horses
* suprascapular nerve: 11,
* axillary nerve 2
Most horses with peripheral neuropathy of a forelimb returned to **athletic soundness following an adequate period of rest.**
Horses with lesions of a **radial nerve** alone or in association with other nerves typically required **longer recovery times** than did those with predominant injuries of a suprascapular nerve.
59
Concurrent Equine Degenerative Myeloencephalopathy and Equine Motor Neuron Disease in Three Young Horses
2016
Conclusion
**EDM and EMND can occur concurrently in young related horses in association with an underlying a-TP deficiency.**
Both NAD/EDM and EMND in horses are associated with a temporal deficiency in a-TP but
* EDM considered to be genetic (currently proposed mode of inheritance in the Quarter Horse as autosomal dominant with incomplete penetrance)
* EMND acquired
60
eNAD/EDM:
definition
experimental antemortem tests
Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy () is a neurodegenerative disorder affecting genetically predisposed foals maintained on an α-tocopherol (α-TOH) deficient diet.
Currently no antemortem diagnostic test for eNAD/EDM is available.
**Study:** in Spinal Cord tissue samples _(Post mortem),_ **targeted markers of cholesterol oxidation**, including 7-ketocholesterol, 7-hydroxycholesterol, and 7-keto-27-hydroxycholesterol **were significantly increased with eNAD/EDM**
**NOT in CSF or serum**
**NO**
61
cervical vertebral osteosarcoma
One report describes a 2-year-old colt presented with sudden-onset ataxia in which a cervical vertebral osteosarcoma causing severe compression of the spinal cord was diagnosed.
Normally very rare
Dx: radiography and CT: Osteolytic and osteoscleroticc lesions. Laboratory analyses of the blood and the CSF tap showed only mild and unspecific changes.
some case reports of surgical extraction in other locations but most horses are subjected to euthanasia due to the locally invasive and destructive nature of the tumour
62
Factors associated with outcome in 94 hospitalised foals diagnosed with neonatal encephalopathy
frequent clinical signs
survival
variables associated with nonsurvival
most frequently identified clinical signs included:
* abnormal udder seeking (59%),
* abnormal suckle (55%),
* inability to stand (42%),
* abnormal gastrointestinal motility (37%),
* abnormal consciousness (34%) and seizure activity (22%).
Survival: 75 (79.8%) foals survived to be discharged from the hospital and 19 foals died or were subjected to euthanasia.
**Variables significantly associated with nonsurvival**
* high serum total calcium concentration at admission
* low serum activity of ALP at admission
* recumbency,
* number of concurrent diseases, and
* use of vasopressors/inotropes. suggesting that persistent hypotension is associated with nonsurvival in the current population
* concurrent disease
63
Sensitivity of radiography and radiographic myelography for vertebral canal stenosis
alternative?
**_Survey radiography :_** 42 and 63% for vertebral canal stenosis identified with intravertebral ratio (IVR) and DJD when compared with necropsy.
**Misdiagnosis of compressive lesions with survey radiography alone occurs in**
* **30%-60% of cases compared with radiographic myelography, and**
* **61% of cases compared with necropsy**
**_radiographic myelography_** in a multicenter study, radiographic myelography had a 68% correlation with necropsy findings
ALTERNATIVE: Computed tomography myelography
64
leading causes of spinal ataxia reported for horses in the eastern United States.
CVCM and eNAD-EDM
65
Postmortem diagnoses of spinal ataxia in 316 horses in California
"horses with eNAD-EDM were 2.95 times as likely to have been..."
**AQHs**,
a breed known to have breed-specific diseases such as hyperkalemic periodic paralysis, hereditary regional dermal asthenia, glycogen branching enzyme deficiency, type 1 polysaccharide storage myopathy, and malignant hyperthermia
_a breed predisposition to eNAD-EDM had not been reported before the present study_
66
α-tocopherol metabolism in horses with equine neuroaxonal dystrophy
* **aberrant vitE metabolism** in QHs with eNAD/EDM, defined primarily by increased **α-TOH metabolism** in serum and urine, after a PO dose of RRR-α-TOH.
* **higher urinary α-CEHC concentrations at similar serum α-TOH concentrations**. (Similar to results obtained in human patients with AVED Ataxia with Vitamin E deficiency)
* **increased hepatic expression of CYP4F2**, the major metabolizer of vitE, was observed in eNAD/EDM-affected horses across breeds. -\> Enhanced metabolism of α-TOH would lead to a higher α-TOH requirement in eNAD/EDM-affected horses.
67
Treatment of temporohyoid osteoarthropathy in horses
* **medical:** reducing inflammation and providing analgesia through administration of NSAIDs, corticosteroids, gabapentin, and antimicrobials
_medical management doesn't work or risk for acute fracture of the petrous temporal bone:_
* **surgical:**
* **partial stylohyoidectomy:** complications such as laceration of the lingual artery, hypoglossal neuropathy, transient dysphagia, stylohyoid bone regrowth, and permanent problems with prehension when performed bilaterally, partial stylohyoidectomy has been replaced with
* **ceratohyoidectomy:** complications: iatrogenic trauma to the ipsilateral hypoglossal nerve, linguofacial vein, and branches of the lingual nerve owing to their close association with the proximal aspect of the ceratohyoid bone
* **_experimental: successful basihyoid-ceratohyoid disarticulation of 6 horses in standing and sedated horses_**
* **Prognosis for survival:**
* good to excellent after surgical intervention
* fair for those treated with medical management alone
68
Toxoplasma gondii seroprevalence and association with equine protozoal myeloencephalitis: A case–control study of Californian horses
association between high T. gondii titres and clinical signs compatible with EPM is potentially reflective of toxoplasmosis in equines. Serologic testing of cerebrospinal fluid and isolation of T. gondii in EPM suspect cases should be considered. Future studies investigating the relationship between T. gondii and EPM are warranted.
69
Cerebrospinal fluid Lyme multiplex assay
Positive Lyme multiplex results were _common in horses with neurologic diseases and did not adequately differentiate horses with neuroborreliosis from horses with other disorders._
## Footnote
**Cerebrospinal fluid Lyme multiplex assay results are not diagnostic in horses with neuroborreliosis**
70
If a tapetal reflex can be visualised through retroillumination (shining a light at arm’s length into the eye and looking for the tapetal reflection), the cause of blindness can be localised
either to the retina or the visual pathway. If the fundus appears normal, a neurogenic cause of blindness should be strongly suspected.
71
In the absence of facial nerve dysfunction or cerebellar disease, loss of menace response indicates
severe visual loss.
72
The pupillary light reflex test...
= brainstem reflex that tests
* the visual components of the eyeball and the central visual pathway to the level of the midbrain (mesencephalic pretectal nuclei).
* motor response requires oculomotor nerve integrity from the oculomotor nuclei in the midbrain through the orbital fissure into the periorbita and ciliary ganglion, as well as short ciliary nerves from the ganglion to the eye.
* Due to decussation of neurons at the optic chiasm and again at the caudal commissure, light directed into one eye stimulates both oculomotor nerves such that pupillary constriction should occur in both eyes.
73
Lesions that destroy the retina or optic nerve in one eye cause
blindness with a normal to slightly dilated pupil (due to light entering the normal eye and stimulating both oculomotor nuclei). If light is directed into the blind eye, neither pupil constricts;
74
Retrobulbar lesions often affect
both the optic nerve and oculomotor nerve of one eye; the affected eye will be blind with a dilated pupil, and light directed into the affected eye does not cause constriction in either eye, whereas light directed into the unaffected eye causes constriction only in that eye
75
Unilateral forebrain lesions in the optic tract, lateral geniculate nucleus, optic radiation or visual cortex cause
**blindness in the CONTRALATERAL eye**
because of the degree of decussation in the optic chiasm. Pupillary light reflexes generally remain normal in both eyes. Bilateral forebrain lesions cause bilateral blindness with preservation of pupillary light reflexes.
76
Causes of neurogenic blindness in the horse
* Traumatic optic neuropathy most commonly occurs after head trauma sustained during falls or collisions (Martin et al. 1986). One common scenario is the horse that rears and flips over backwards (due to tying, fear or another reason), causing shearing or severing of the optic nerves as the brain moves away from the fixed, intracanalicular optic nerves
* One important anatomical feature to remember is that the optic nerves are located immediately dorsal to the sphenopalatine sinuses, which are relatively thin-walled. Infections, inflammatory processes, granulomas or neoplasia in the sphenopalatine sinuses can cause blindness that is slowly progressive or acute in onset (Barnett et al. 2008; Radcliffe et al. 2016) but also other cranial nerves affected: III, IV, V and VI
* ischaemic optic neuropathy is associated with sudden hypoxia as might occur during severe hypovolaemia or hypotension (as can occur with acute severe blood loss) or surgical occlusion of the external and internal carotid arteries (Freeman et al. 1990; Hardy et al. 1990)
* Optic neuritis can occur due to extension of local inflammatory disease or primary central nervous system diseases
* meningitis can affect the optic nerves, as can CNS neoplasia. Finally, toxic insults have been implicated in optic nerve degeneration
* Metabolic encephalopathies are probably the most common cause of bilateral central blindness and can occur due to hepatic disease, renal disease, intestinal disease (hyperammonemia), electrolyte derangements or other metabolic abnormalities.
* Rarely, horses show transient (\<5 days) central blindness following routine myelography
* Any disease that causes seizure activity can cause post-ictal central blindness that might persist for several days
* Unintentional intracarotid injections can cause acute cerebral toxicity or infarction of the ipsilateral forebrain resulting in contralateral blindness.
77
presenting complaints of Lyme borreliosis
* Cranial or peripheral neuropathies were common. Facial nerve palsy, as observed in 4/16 of the horses in this study and in 3/7 previously reported cases of equine NB,6,7 occurs in 8% of human NB cases.24 Dysphagia was frequently observed and has been described in the human literature in association with Borrelia brainstem encephalitis.25 Histologic findings from this report indicate that the cause of dysphagia might be multifocal including cranial neuritis, guttural diverticulitis, and tongue and esophageal myositis. Recurrent laryngeal nerve paralysis has also been reported as a rare complication of human NB that can result in dysphonia and respiratory failure requiring tracheostomy.26–28 Fever and neck stiffness (noted in 2 and 6 horses, respectively) were present in 15% of the 118 patients with acute NB.29
* Uveitis was the most frequent extraneural manifestation of Borrelia infection. Five cases of equine uveitis associated with Borrelia have been reported
78
Newborn foal with atypical myopathy
story
theories
* foal’s dam was diagnosed with AM in the 6th month of gestation based on clinical signs of a myopathy, elevated serum activity of creatine kinase, metabolomic analysis and the presence of methylenecyclopropyl acetyl carnitine (MCPA-carnitine) in the blood. At the time of delivery, the mare was grazing on a pasture near sycamore trees but was free of clinical signs of AM.
* Two theories could explain this observation (a) hypoglycin A or its metabolites accumulated in the mare’s placenta with consequent transfer to fetus or (b) these compounds were secreted into mare’s milk.
79
The lack of clinical disc disease in the horse is attributed to
the absence or poorly developed nucleus pulposus, and relatively thin width of the intervertebral discs. Equine intervertebral discs have a central fibrocartilaginous area that becomes more fibrous peripherally and is relatively thin, making horses less susceptible to disc prolapse
80
Somatic innervation of the bladder originates from
m the sacral cord (S1–S2) by way of the pelvic nerve and branches of the pudendal nerve, which also innervate the perineum and external anal sphincter
81
Articular processes joint enlargement has been associated with
vertebral canal stenosis and spinal cord compression in ataxic horses diagnosed with cervical vertebral stenotic myelopathy (CVSM) (cervical vertebral malformation, wobbler syndrome) and with nerve root compression at the intervertebral foramen, leading to local cervical pain, muscle atrophy and thoracic limb lameness
82
Computed tomography and myelography of the equine cervical spine: 180 cases (2013–2018)
the most common pathology reported was...
OA of the APJs at the articulations of C5–C6, C6–C7, C4–C5 and C3–C4.
83
Which imaging modality can be considered the gold standard for studying the central nervous system, including the brain and cranial nerves, as well as the extracranial soft tissues, including the orbit, lymph nodes, blood vessels, muscles and salivary glands.
MRI
84
Which imaging modality can be considered the gold standard for studying the skull bones, the temporomandibular joint, the temporohyoid articulation and teeth. also adequate for studying the nasal passages and paranasal sinuses, being particularly useful for identifying subtle nasal and sinusal osseous wall lesions
CT
85
In 2 retrospective studies involving 34 and 47 horses with traumatic head injury, neurological deficits were most commonly associated with
basisphenoid/basioccipital bone fractures.
86
Who provides sensory innervation to the pharynx
CNIX and CNX
87
dysphagia, right laryngeal paralysis, dysphonia, and lack of a gag reflex 5 days after poll injury
possibly Delayed onset vagus nerve paralysis after occipital condyle fracture
IX and X near the condyle
XI could be damaged too due to proximity
\*In the present case, CNXI function appeared to be intact as evidenced by the lack of electromyographic changes over the right trapezoid muscle and the absence of muscle atrophy both clinically and on postmortem examination. The CNs IX, X, and XI share the same outlet from the skull, however once they exit, CNIX and CNX follow a cranio-ventral route. In contrast, CNXI travels caudally soon after leaving the skull.
88
Apart from cranial nerve signs, unilateral CNX damage can also cause
stomach acid secretion disorders and transient delayed gastric emptying
89
MRI and CSF findings in Transient bilateral blindness associated with idiopathic hypertrophic pachymeningitis
which other test is indicated for definitive diagnosis?
CSF: Basophilic inflammation
MRI diffuse, marked thickening and moderate contrast enhancement of the pachymeninges overlying the cerebrum + apparent increase in cerebrospinal fluid (CSF) volume
biopsy of the meninges
90
Accurate antemortem EPM diagnosis requires
evidence of intrathecal antibody production against S. neurona or N. hughesi.
91
How can SAA and CRP aid in the diagnosis of EPM?
Neither SAA nor CRP in serum or CSF aid diagnosis of EPM
92
The most likely differential diagnoses for enlargement of the pituitary gland in the horse, seen on CT images, are
age-related changes or melanotrope hyperplasia and macroadenoma formation in the pituitary pars intermedia
.....
abscess formation possible
93
On impact, the compressive forces are transmitted through the brain causing
compression of the brain against the lagging or opposite surface of the skull, resulting in a larger contrecoup lesion at that location.
94
how can ataxia grading be objectified?
Motion capture can objectively aid the assessment of horses with ataxia. Furthermore, blindfolding increases variation in distal pelvic limb kinematics making it a useful clinical tool.
For horses with a median ataxia grade ≥2, coefficient of variation for the location of maximum vertical displacement of pelvic and thoracic distal limbs generated good diagnostic yield. The hoofs of the thoracic limbs yielded an Area Under the Curve of 0.81 with 64% sensitivity and 90% specificity. Blindfolding exacerbated the variation for ataxic horses compared to non-ataxic horses with the hoof marker having an AUC of 0.89 with 82% sensitivity and 90% specificity.
95
surgical TTRM of cervical vertebral compressive myelopathy and new techniques
different ventral interbody fusions
new: placement of an interbody fusion device and polyaxial pedicle screw and rod construct for cervical vertebral fusion (19) but only 10 horses
96
EquiPENS :
success rates in idiopathic headshaking and where is it placed?
The recently developed, equine specific, neurostimulation device EquiPENS1 has now been used in over 130 TMHS horses with approximately **50% successfully returning to the previous level of activity**
. Ultrasonographic guidance is used to direct the probe percutaneously such that it lies approximately 1 mm superficial to the infraorbital nerve prior to stimulation (Roberts et al. 2016)
97
What is the theory behind Therapeutic application of electricity for pain
**gate control theory** of pain by Melzack and Wall (1965)
**substantia gelatinosa in the dorsal horn of the spinal cord**: = gate control system, which modulates the synaptic transmission of nerve impulses from peripheral fibres to the central nervous system.
* **Small nociceptive A-d and C** fibres hold the ‘gate’ in an open position,
* **stimulation of large mechanoreceptive A-b** fibres by touch, pressure or vibration close the ‘gate’ and _inhibit pain transmission to the brain._
Small nociceptive fibres: _higher activation threshold_ than larger mechanoreceptive fibres =\> _selective low level stimulation of mechanoreceptors can prevent or reduce pain transmission_. Activation of these large A-b fibres _recruits inhibitory interneurons within the substantia gelatinosa_ of the spinal cord which exert their inhibitory action on both large and small diameter fibres synapsing higher up the spinal cord.
additional activation of the descending inhibitory pathway =\> release of endogenous opioids and alterations of many other neuro-excitatory or inhibitory compounds
98
When the poll strikes a hard surface such as pavement during rearing and flip-over injury
the **nuchal crest acts as a pivot** causing the _head to flip into extension resulting in sudden and dramatic stretch of the rectus capitis ventralis muscles_. This often leads to a fracture of the **basioccipital and basisphenoid bones** and tearing of the adjacent blood vessels which may include the occipital artery causing haemorrhage into the guttural pouch and ear canals.
99
MMEP cutoff values for detection of spinal cord dysfunction in horses
Transcranial magnetic stimulation (TMS) and recording of magnetic motor evoked potentials (MMEP) can detect neurological dysfunction in horses
To detect spinal cord dysfunction caused by compression, the optimal cutoff for thoracic limbs remained 22 milliseconds, while it increased to 43 milliseconds in pelvic limbs (sensitivity, 100% [100%-100%]; specificity, 100% [100%-100%] for thoracic and pelvic limbs).
100
compare diagnostic accuracy of TMS, cervical radiography, and neurological examination for spinal cord dysfunction/compression and ataxia
**Sensitivity and specificity**
* **of neurological examination**: 97.6 and 74.7%
* **of radiography** 43.0 and 77.3
* **of transcranial magnetic stimulation** 87.5 and 97.4 For TMS, the highest accuracy was obtained using the minimum latency time for the pelvic limbs (Youden's index = 0.85).
=\> combination of neuro exam and TMS best
101
sensitivity
= ability to correctly identify diseased
102
specificity
what if its low?
ability to detect non diseased
if it is low you have many false positives
103
reported atypical form of EMND
additionally to usual clin signs: Reduced tongue tone associated with degeneration of the hypoglossal nerve nucleus
normally the disease affects many cranial nerve nuclei (histologically) but it is suspected that cranial nerve signs do not appear bc only a certain percentage of neurons are damaged
achtung geht normalerweise auf type I muskeln und zunge ist typ 2!!!
104
3 main post mortem findings to diagnose EMND
* **denervation atrophy** of muscles with a higher prevalence of type I myofibres,
* lipopigment accumulation in endothelial cells
* degeneration of neuronal somata and axons
105
Prevalence of headshaking within the equine population in the UK(owner questionaire)
The estimated prevalence of owner-reported headshaking in the sample population of horses (n = 1014), within the last year, was 4.6% whereas 6.2% of horses were reported by their owners to have shown signs of headshaking at any time-point since ownership.
## Footnote
There was no association of sex or breed. Nineteen percent of headshaking horses were reported to show headshaking at rest.
Fewer than one-third (30.2%, n = 19) of headshaking horses had been examined by a veterinarian for headshaking. Of horses seen by a veterinarian, the cause for headshaking remained unknown in the majority of cases (57.9% responses) and trigeminal-mediated headshaking was reported as a diagnosis in just one case
106
A pilot study of optical neuronavigation-guided brain biopsy in the horse using anatomic landmarks and fiducial arrays for patient registration
Optical neuronavigation using the Brainsight Vet 2 system is feasible in horses and, based on our preliminary data, the use of anatomic landmarks appears to be a feasible option for registration. Optical neuronavigation should be considered when performing brain biopsies or surgical procedures in horses that may require a high degree of accuracy, such as surgical treatment of Cushing's disease and biopsy or resection of inflammatory lesions, granulomas, or other masses, and may allow such procedures to become more feasible
107
The diagnosis of EPM relies heavily on the clinical examination. The sensitivity and specificity of the Western blot analysis for antibodies to S. neurona in cerebrospinal fluid (CSF) have been reported to be
89 and 89%, respectively, based on comparison to postmortem evaluation in severely affected horses.
108
Interobserver Variation in the Diagnosis of Neurologic Abnormalities in the Horse
The agreement among observers was either good or excellent for 80% of horses when evaluating for the presence or absence of neurologic abnormalities.
* _best agreement:_ presence or absence of neurologic signs, lameness, ataxia, and truncal sway,
* _worst agreement:_ assessing muscle atrophy, spasticity, and severity of neurologic deficits
109
intracranial infections in the literature: causing agents?
Previous reports have attributed intracranial infections in 20 horses to **abscesses caused by Streptococcus equi spp. equi and spp. zooepidemicus (50%)** **or mixed bacterial and fungal infections of the calverium** extending from _trauma, paranasal sinusitis, pituitary gland abscesses and/or pneumonia (50%)_.
Curiously, infection with **Streptococcus equi spp. equi and spp. zooepidemicus was more likely to result in metastatic cerebral abscessation ,** while infection with other organisms was more likely associated with extension of sinus infections or trauma or possibly associated with chronic pneumonia.
110
prognosis of brain abscess/intracranial infection
reports demonstrate that the prognosis is guarded (4/20 survived) and poor with medical treatment alone (0 survived).
111
oral supplementation of XXX decreases headshaking
6 headshakers and 6 controls:
Combined magnesium-boron supplementation induced the highest IRR reduction (64%) in headshaking behavior when compared to hay diet only. Similarly, magnesium-boron supplementation had the greatest IRR reduction (36%) in headshaking behavior when compared to a diet containing pelleted feed. The most severely affected horses had the most benefit to supplementation providing magnesium
112
Magnesium requirements of the horse
The requirement for magnesium in horses is 13 mg/kg BW and for an average 500 kg horse, the requirement would be 6.5 g of magnesium a day
113
presumed mechanisms of action for mg in headshaking
1500-2000 mg/kg of PO MgSO IV led to a 29% reduction in head-shaking rate
* acts as a blocking agent to N-methyl-D-aspartate (NMDA) receptors, which have been shown to have an effect on trigeminal neurons
* inhibit Ca2+-dependent presynaptic excitation-secretion coupling
* magnesium has been utilized in anesthesia as an analgesic agent (effect unknown)
114
Headshaking and LH
: Horses affected with headshaking did not have significant differences in circulating LH during the late summer as compared to control horses.
115
Main findings of the study: Management of equine ataxia caused by cervical vertebral stenotic myelopathy: A European perspective 2010–2015
Among treated horses, 69% of conservatively managed and 43% of surgical cases returned to use. Surgical cervical vertebral interbody fusion using threaded kerf-cut cylinders resulted in sufficient stabilisation and thus, remains a reliable technique particularly in more severely affected horses.
116
intrathecal pain management for laminitis cases
Caudal epidural administration of a mixture of opioids and ɑ2-agonists is now routinely used to provide analgesia to the pelvic limbs. More recently, the use of larger volumes to extend the analgesic effect to the thoracic limbs has also been advocated (
117
caudal epidural administration of morphine and detomidine in a pony - case report side effects
Presumed generalised seizure
theory is the sudden increase in epidural and intracranial pressures (injection over 90s) precipitated the seizure. Take home message:
injection of large volumes over several minutes. to facilitate this, use a prolongation to minimise needle movement
118
prevalence of morphologic variation at C6 and C7 and what does that mean clinically
28.6% in one study concerning warmbloods
Homologous morphologic variation is common in the caudal cervical spine of Warmbloods. This variation does not appear to be associated with clinical signs and in fact is less frequent in clinical cases than in control animals
119
Use of threshold testing for tactile sensory, mechanical and thermal nociceptive stimulations in the face of horses
The combined application of all three modalities enables comprehensive evaluation of the equine trigeminal sensory function with good reliability
120
What is myokymia
muscle twitching
continuous undulating movements
Myokymia is a clinical sign of neuromyotonia.
121
Neuromyotonia is clinically characterized by
a combination of muscle twitching or myokymia, persistent muscle contraction, muscle stiffness, impaired muscle relaxation, and continuous electromyographic activity.27–29 Clinical and electromyographic examinations are important to differentiate neuromyotonia and myokymia, although these clinical entities can occur simultaneously.
122
differentiate neuromyotonia and myokymia
Electromyographic recordings in cases of neuromyotonia disclose spontaneous, continuous, irregularly occurring doublet, triplet, or multiplet single or partial motor unit discharges, firing at a high intraburst frequency (30-300 Hz). Spontaneous discharges at the highest frequencies (150-300 Hz) that occur in prolonged bursts, and which begin and end abruptly and often wane in amplitude, have been called neuromyotonic discharges. Each burst of electrical activity usually occurs irregularly, with variable interburst frequencies (from 100 milliseconds to \>10 seconds). Myokymic discharges tend to occur at lower frequencies (often \<60 Hz), often as doublets, triplets, or multiplets, in short semi-rhythmic bursts, followed by a few seconds of silence.6,28 The horse described here showed clinical and electromyographic signs of myokymia and neuromyotonia, and a mixed neurogenic-myopathic histological pattern also was observed.
123
clinical signs of myotonia
Affected animals have gait impairment, muscle hypertrophy, stiffness, and hypertonicity. Myotonia can occur concurrently or without muscular dystrophy.
124
How does myotonia look like during EMG?
Myotonic potentials are a common finding in these animals and represent spontaneous repetitive discharges with waxing and waning amplitudes and frequencies
125
What is Dystrophic myotonia
a progressive disorder initially characterized by generalized myotonia with hypertrophy and hypertonicity of the larger hind limb and forelimb proximal muscles. It is associated with a dystrophic histological pattern (ie, sarcoplasmic masses, ringed fibers, moth-eaten fibers, adipose and connective tissue inflammation). A few cases have been described in horses.
126
