Neurology Flashcards
0
Q
Describe the order of the neurological exam?
A
- Sensorium. 2. Cranial nerves. 3. Gait. 4. Postural reactions. 5. Spinal reflexes.
1
Q
Why do a neurological examination?
A
To determine if the nervous system is affected in a disease process, to establish an anatomic diagnosis - forebrain (prosencephalon), pons and medulla, cerebellum, C1-C5 spinal cord, C6-T2 spinal cord, T3-L3 spinal cord, L4-Cd Spinal cord, neuromuscular.
2
Q
What are the signs of forebrain disease in sensorium?
A
Check behaviour, mental status. Changes in sensorium may be dullness, lethargy, obtundation, semicoma, stupor, coma, central blindness, abnormal limb placement, circling (often towards the lesion), seizures.
3
Q
How do you check the cranial nerve reflexes?
A
Menace - check vision and pupils (may be ANiscoria) Check PLR
Eye position/movement
Nystagmus - named after the direction of the fast phase. fast phase away from lesion. horizontal and rotatory nystagmus - peripheral disease. Vertical nystagmus - central lesion.
Palpebral response
Nasal septal response
Muscles of mastication
Gag reflex.
4
Q
What may be present in the gait on a neurological exam?
A
Vestibular/cerebellar/GP ataxia
UMN/LMN paresis;
UMN - delay in the onset of protraction/spasticity
LMN - inability to support weight
Ataxia - general proprioception, vestibular, cerebellar
5
Q
Which postural reactions should be checked in a neurological exam?
A
Palpate limbs, paw placement, hopping responses on Pelvic and thoracic limbs and hemiwalking.
6
Q
Which spinal reflexes should be tested on neurological examination?
A
Cutaneous trunci reflex, perineal reflex, patellar reflex, withdrawal reflex/nociception.
7
Q
What are the clinical signs of forebrain Disease?
A
Abnormal behaviour, head pressing, staring at walls, getting stuck in corners, abnormal mental status, circling in wide circles towards the side of the lesion, continuous pacing, normal gait, Contralateral postural deficits, central blindness (contralateral to the lesion), sensory deficits (contralateral to the lesion), generalised or/and partial seizures, adversive (hemineglect) syndrome, hippus or pupillary athetosis, abnormal temperature regulation, abnormal appetite, abnormal sleep wake cycle, endocrine disturbances - diabetes insipidus, diabetes mellitus, hyperadrenocorticism, acromegaly (excess of growth hormone).
8
Q
What diagnostic procedures an be done for forebrain disease?
A
Physical and neurological examination, MDB, EEG, CT scan or MRI, CSF analysis, infectious disease titres on serum/CSF, biopsy.
9
Q
Describe storage diseases of the forebrain?
A
Degenerative disorders characterised by the accumulation of different products of cell metabolism within lysosomes. One or more defective enzymes. Accumulation of by products leads to cellular and organ dysfunction. Progressive myoclonic epilepsy (lafora diseasE) in miniature wire haired dachshuds, beagles and basset hounds, fucosidosis - english springer spaniels, ceroid lipofuscinosis - english setters, broder collies, tibetan terriers.
10
Q
Describe hydrocephalus
A
Increased CSF volume in dilated ventricular cavities. Compensatory hydrocephalus or Ex vacuo. Non communicating or obstructive hydrocephalus, communicating hydrocephalus - increased production of CSF or decreased CSF reabsorption. Congenital hydrocephalus - chihuahua, Yorkshire terrier, pomeranian, pekingese, english bulldog, pug. Presents - large domed head, lateral or ventrolateral strabismus, persistent sutures and fontanelles, loss of trained habits, seizures, blindness.
11
Q
Describe the diagnosis and treatment of congenital hydrocephalus?
A
EEG, brain ultrasound through open fontanelle, skull radiographs, brain ct scan or MRI. Treat with furosemide, corticosteroids, acetazolamide. Or surgically with ventriculoperitoneal shunt.
12
Q
Which metabolic disorders can cause diseases of the forebrain?
A
Hypoglycaemia, organ dysfunction - hepatic or uraemic encephalopathy. Endocrine diseases - diabetes mellitus, hypothyroidism, hyperthyroidism. Electrolyte imbalances - hyponatraemia, hypernatraemia, hypophosphtaemia, hypercalcaemia, acidosis or alkalosis.
13
Q
What is hepatic encephalopathy?
A
seen with Acquired (acute or chronic liver failure), or congenital portosystemic shunt. Toxic substances from intestinal degradation are not metabolised by the liver or bypass it, reaching the brain. Causes depression, head pressing, tremors, seizures, central blindness and ataxia. Diagnosis is with bile acids test, abdominal ultrasound, abdominal ct scan, positive contrast portopgraphy, brain MRI, Medical treatment: low protein diet, antibiotics and lactulose, surgical ligation.
14
Q
Describe Neoplastic diseases of the brain seen in dogs
A
Primary tumours - glioma (astrocytoma and oligdendroglioma), meningioma
Secondary tumours - nasal adenocarcinoma, pituitary macroadenoma, metastasis from mammary prostatic or pulmonary carcinomas or haemangiosarcomas.
15
Q
Describe neoplastic diseases of the brain seen in the cat
A
Primary tumours - meningioma
Secondary tumours - metastatic carcinoma, lymphosarcoma, squamous cell carcinoma, nasal adenocarcinoma.
16
Q
Which infectious organisms cause diseases of the forebrain?
A
Viruses - Rabies, pseudorabies, CDV, FIP, canine herpes, WNV
Protozoa - toxoplasmosis, neosporosis
Rickettsia - RMSF, Ehrlichia canis
Fungi -Cryptococcis, blastomycosis, histoplasmosis, coccidiomycosis.
Parasites - cuterebra, coenurus, cystercercs, dirofilaria immitis, toxocara canis.
Bacteria - pasteurella spp, s aureus, s. epidermis
Spirochetes - leptosirosis, (Lyme disease).
Protothecosis.
17
Q
What signs does Canine distemper virus causE?
A
In young dogs, CNS signs may occur weeks to months after recovery from systemic illness, myoclonus: rhythmical jerking movements of muscle groups.
18
Q
how does Feline infectious peritonitis affect the brain?
A
the dry/non effusive/granulomatous form. CSF _ mixed pleocytosis (predominantly neutrophils) PCR on CSF. MRI or CT brain - hydrocephalus, meningitis and choroiditis.
19
Q
Describe inflammatory diseases of the forebrain?
A
Meningo encephalitis of unknown origin - necrotizing minigo encephalitis of pug and maltese dogs and Yorkshire terrier encephalitis - fore brain signs.
Granulomatous meningo encephalo-myelitis - caudal fossa (cerebellum + pons/medulla) and forebrain signs.
20
Q
What substances can cause toxic diseases of the forebrain?
A
Ethylene glycol toxicity, lead poisoning
21
Q
Describe vascular diseases of the forebrain?
A
Diffuse cerebral ischaemia - caused by cardiopulmonary arrest, anaesthetic accident, severe cerebral edema following a toxic or traumatic event.
Focal cerebral iscahemia - i.e thrombus, embolism or thromboembolic diseases caused by cardiac disorders, septic or neoplastic emboli,hypothyroidism inducing atherosclerosis (RARE), migrating parasites.
Diffuse or focal haemorrhages caused by trauma, neoplasia, coagulation disorders e.g rodenticide intoxication, severe hepatopathy, vasculitis, hypertension (secondary to hyperadrenocorticism, renal failure).
22
Q
Describe the pathophysiology of head trauma
A
Primary injuries - fractures, blood vessel disruptrion, tearing or crushing of parenchyma. Occur at the time of trauma. non reversible.
Secondary injuries - ischaemia, excitotoxicity, cerebral edema (vasogenic edema, cellular or cytotoxic edema), haemorrhage. hours to days after trauma - coontrollable.
23
Q
Describe what fills th intracranial space?
A
80% brain, 10% blood, 10% CSF, encased in bone, intracranial pressure is the pressure exerted by tissues and fluids within the cranial vault. Causes of increased intracranial pressure in head trauma : intracranial haemorrhage, cerebral edema, systemic hypotension, hypoxaemia.
24
What is cushings reflex?
Increased intracranial pressure > cerebral schaemia> increase in heart rate and systemic extra cranial vasoconstriction > reflex systemic hypertension to increase cerebral perfusion > increased systemic arterial blood pressure stimulates baroreceptor reflex inducing bradycardia.
25
What are the goals of head trauma management and how is neurologic assessment done?
Maintain ventilation, avoid hypotension, prevent/treat cerebral edema, treat increased ICP. Neurologic assessment - state of consciousness, breathing pattern, size and responsiveness of pupils, Occular position and movements, skeletal motor responses.
26
What are the different levels of consciousness, breathing patterns and occular positions that may be noted in neurological exam after head trauma?
alert, depressed, demented, stuporous, comatose.
Cheyne-stokes respiration (forebrain)
Central neurogenic hyperventilation (mesencephalon/pons)
Apneustic breathing or cluster breathing (pons/medulla)
Ataxic respiration (respiratory centres in medulla).
Abnormal oculocephalic reflex or physiologic nystagmus, strabismus.
27
What signs may b e present with brainstem injuries?
Abnormal oculocephalic reflex (physiological nystagmus), bilateral unresponsive miotic pupils, mydriasis or asymmetrical pupils, strabismus and other cranial nerve deficits, abnormalities or changes in respiratory pattern.
28
What is the difference between decerebrate rigidity and decerebellate rigidity?
Decerebrate - unconsciousness, abnormal pupillary function,, opisthotonus, extension of thoracic and pelvic limbs.
Decerebellate rigidity - alert, normal pupillary function, opisthotonus, extension of thoracic limbs, extension or active flexion of pelvic limbs.
29
What are the clinical signs of Increased ICP?
Nausea/ovomiting, decreased PLR, decreased level of consciousness, Cushings reflex (hypertension & bradycardia) abnormal respiratory pattern, increased limbs' extensor tone.
30
What are epileptic seizures?
abnormal brain function, synchronous activation of many neurons or excessive activation of few neurons, in the cerebral cortex. usually self limiting. Epilepsy is a chronic neurologic condition, wit recurrent epileptic seizures.
31
What are convulsions?
Have a generalised motor component, excessive, abnormal muscle contractions, usually bilateral.
32
What is ictus?
A sudden neurologic occurence, such as a stroke or an epileptic seizure
33
What is the prodromal stage and pre ictal phenomenon?
behavioural changes or autonomic signs that may precede an observable seizure.
34
What is the post ictal phenomenon?
A transient clinical abnormality of the CNS function that appears or becomes more evident when the clinical signs of the seizure have ended e.g disorientation, ataxia, central blindness behavioural changes.
35
What are generalized seizures?
Have involvement of both the cerebral hemispheres - tonic clonic seizures, clonic, tonic, atonic or absence seizures.
focal or partial seizures activation of only part of a cerebral hemisphere - simple partial seizures (conscioussness is not impaired), complex partial seizures (with impairment of consciousness.)
36
What is a cluster of seizures?
> two seizures in a 24 hour period or over 2-3 consecutive days.
37
What is status epilepticus?
A seizure that shows no clinical signs of arresting after 5-10 minutes of activity or recurrent seizures with no recovery between them.
38
What is idiopathic epilepsy?
Recurrent seizures, no identifiable cause, genetic/familial predisposition, age dependent.
39
What is symptomatic epilepsy?
Result of identifiable intracranial or extracranial disease. intracranial causes such as brain tumors, encephalitides, infarcts.
Extracranial diseases such as toxic or metabolic disorders.
40
What is a seizure?
A seizure is originated by an imbalance of excitatory and inhibitory influences on the cerebral neurons.. When too many cells in the cerebral cortex become too excited a seizure can result. there is a seizure threshold. There is a seizure foci - paraoxysmal depolarisation in a neuron. There is spread of activity to the surrounding neurons. Propagation of seizure activity to cortical areas by axonal conduction. Generalization of seizure activity through diencephalon and corpus callosum.
41
What signs may be present in a generalised tonic clonic seizure?
Loss of conscioussness, opisthotonus, piloerection, chewing movements, face twitching, midriasis, salivation, apnea, lateral recumbency, urination/defecaetion. tonic phase is stiff legs and clonic phase is paddling legs.
42
Which dogs are predisposed to idiopathic epilepsy?
Between 105 yerars, regular intervals initially > 4 weeks.Genetic basis of epilepsy in beagles, german shepherd dogs, keeshonds, golden and Labrador retrievers, bernese mountain dogs, tervuren elgian shepherds, viszla, english springer spaniels, border collies, finnish spitz dogs.
43
What is the DDx for Idiopathic epilepsy?
Syncope (cardiac arrythmias, induced by changes in posture or excercise) sleep disorder (short duration and rapid reovery, occurs only during sleep, attacks can be interupted by awakening), Obsessive compulsive behaviour (prolonged duration of signs, behaviour can be interupted, no impairment of conscioussnes), scotty cramp (breed specific, excercise or stress induced), canine distemper myoclonus (continuous abnormal movements, no impairment of consciousnes), myasthenia gravis (gradual onset and recovery, no loss of conscioussness), vestibular disease (prolonged duration of signs), tremor disorders (prolonged duration of signs, no impairment of consciousness) Narcolepsy/cataplexy (attacks often induced by ecitement, food, play, reversed by external stimulation.
44
How is IE diagnosed?
```
Signalment
History
Physical and neurological examination
CBC, biochemical panel, UA
Bile acids, lead level, serological studies, thyroid panel, EEG, CSF analysis, CT scan or MRI.
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45
What is the aim in treatment of IE and the expectations?
Reduction in frequency and intensity of seizures
Rarely will become seizure free
owner should keep a seizure log
anti epileptic therapy must have regular administration, do not stop suddenly AE therapy, has side effects, kindling phenomenon
46
How can epilepsy be treated by vagal nerve stimulation?
A surgically implanted device (neck area) prevents seizures stimulating the left vagal nerve and desychronizing the cortical neurons. Reasonable margin of safetly. well tolerated. reduction in seizure frequently in some dogs.
47
What medicines should not be used in epileptic animals??
Some drugs such as metoclopramide, penicillin, chloramphenicol, Enrofloxacin and estrogens or testosterone may lower the seizure threshold. Phenothiazines are reported to induce seizures, however acepromazine appears to be safe for use in dogs with epilepsy.
48
What is the treatment of status epilepticus?
Stop the seizure - use diazepam per rectum to stop a seizure. May repeat 2 more times at 5 minute intervals. Injectable form of diazepam may be more effective than supositories. Alternatives with no IV access, midazolam or dexmedetomidime Im. Place an IV catheter. collect blood for haematology and biochemistry and antiepileptic drug serum level in case the patient is already receiving AED. If diazepam stops the seizure only for a short period of time - use phenobarbitone and repeat 3 more times at 1-6 hour intervals. Levetiracetam also can be used for patients with hepatopathy or PSS. If 3 doses of diazepam are not sufficient to stop the seizure - administer propofol then switch to a CRI of propofol. Monitor cardio respiratory function closely and be ready to intubate if necessary.
49
What are the requirements for anti epileptic drugs?
Successful control of seizures with anticonvulsant drug reflects a balance between achieving seizure control and minimising side effects.May only be able to increase the seizure interval. BEneficial since seizures can lead to additional seizuring.
50
Describe the drug requirements for status epilepticus?
Rapid onset of action, available for i/v usage, minimal effects on cardiovascular and respiratory systems. e.g diazepam - a benzodiazepine is the D.O.C. Phenobarbital, propofol.
51
What are the drug requirement for maintenance therapy?
Long duration of action (once daily treatment), good oral absorption and passage through the BBB, metabolic tolerance limited, minimal sedation, consistent clinical response, absence of major side effects (hepatotoxicity). All available drugs fail to meet these requirements.
52
What are the mechanisms of action of the anti epileptic drugs?
Enhanced GABA (gamma-aminobutyric acid) synaptic transmission - barbiturates, benzodiazepines, imepitoin.
Potassium bromide - distributes to ECF, crosses neuronal Cl- channels more readily than Cl-. GABA enhances this influx of bromide leading to neuronal hyperpolarization thus bromide stabilises neurone against excitatory input from epileptic foci.
53
Describe the use of phenobarbital for epilepsy
Frequently used in canine epilepsy - first line and licensed. Can be used in cats and horses also. potentiates synaptic inhibition through the GABA receptor. Oral absorption is slow but good it is usually given orally. injectable form also available for status epilepticus management. 25% is excreted unchanged by the kidneys - it acts as a weak acid therefore alkalinisation of urine enhances excretion. the rest is metabolised by oxidative hydroxylation and then glucuronide onjucation. it is a potent inducer of heptatic microsomal enzymes. Effective in about 60-80% of canine epilepsy.
54
Describe the use of imepitoin for Epilepsy?
new, licensed as a sole agent for canine epilepsy. it is a partial agonist with low affinity for the BDZ binding site of the GABA receptor. certain advantages since low affinity and efficacy. it is targeted - only binds when GABA is present. Oral bioavailability is decreased a little with food but doesnt matter as long as consistency is important. Hepatic metabolism (oxidation) and inactive metabolites undergo faecal excretion. There is no induction of liver enzymes. It has a half life about 2 hours so steady state is rapidly achieved.
55
Describe how potassium bromide is used as an anti epileptic drug?
Halide element and causes neuronal hyperpolarization by entering neurons via chloride channels. it is synergistic with phenobarbital (licensed for combo treatment), handled like chloride in the body, excreteed in the kidneys ( no biotransformation) half life in dogs 1 months. Steady state - 3-6 months. dietary chloride will influence half life. High chloride diets increase elimination and derease half life (dry diets e.g hills s/d id h/d). Indications are for with phenobarbital for uncontrolled seizures, dogs with hepatotoxicity, pre existing liver disease, unnaceptable side effects of phenobarbital.
56
Describe the use of diazepam as an anti epileptic drug?
It is a benzodiazepene which enhances the inhibitory effect of GABA in the brain and spinal cord. It is the drug of choice for the management of status epilepticus in the dog and cat. Can be used for long term seizure management in the cat - given orally 12-24hours. It is rapidly metabolised to a variety of active metabolites such as nordiazepam and oxazepam. Species variation on percentage metabolites but metabolites are active. Quite highly bound to plasma protein. Half life has a species variation - 6X longer in cat than dog. Can be given orally or parenterally. Hepatic necrosis in cats seen as early as 5 ays after treatment initiation. This can be rapidly fatal so very serious. Monitor hepatic parameters.
57
Describe the potential for toxicity in all anti epileptic drugs?
Side effects include - sedation, polyphagia, polydipsia, polyuria
High long term doses of phenobarbital can lead to hepatotoxicity
Asthma like symptoms have been reported in cats on KBr. Gingival hyperplasia occurs occasionally in cats. Most dogs receiving chronic anticonvulsant therapy will develop abnormalities in serum biochemistry and hepatic function tests.
58
What should the dosing schedule be for anti epileptic drugs?
Dosage requirements of anti epileptic drug vary between patients and should be determined on an individual basis. Dosage depends on the incidence and severity of seizures. Initial daily dose requirement may have to be increased to maintain blood and brain concentrations as a consequence of metabolic tolerance (liver enzyme induction). Pharmacokinetics data help to establish dialy dosing regimens - good for dog, sparse for cat. For both dog and cat, when complete control of seizures for 6 months, careful stepwise reduction in drug dosage may be attempted.
59
How can anti epileptic drugs be used in combination therapy?
Select drugs from differing classes eg phenobarbital and potassiu, bromide. approx 30% of dog are refractory to phenobarbital or side effects are unacceptable - sedation, hepatotoxicity. Control is particularly difficult in dogs with cluster fits - there is an apparent high incidence of refractory epilepsy in GSDS. Use 2 drugs in combination if a single agent causes toxicity or has failure to control (e.g seizures once per 2 weeks). Avoid irrational combinations e.g phenobarbital and primidone, phenobarbital and phenytoin (metabolic toelrance).
60
Describe epilepsy in the cat
Much less common than in the dog, more often reflects structural disease, less pharmacokinetic data and extrapolation is not ideal, metabolic tolerance to phenobarbital does not occur, KBr has been tried, diazepam has been used for maintenance therapy in the cat - longer half life.
61
What is zonisamide?
A new advance - blocks voltage dependent sodium and potassium channels. it has a half life 15 hours in the dog, In a trial on 13 dogs - it was used as an add on treatment, very epensive, promising results but some suggestion of tolerance.
62
What are gabapentin and pregabalin?
MOA: analogue of GABA but a2 component of calcium channels. they have a short half life, used as an adjunct. Small trial information improvement suggested. Neuropathic pain role in therapy.
63
What is the function of the vestibular system?
it is responsible for maintaining balance, regulating the position of the eyes, trunk and limbs in relation to changes in position of the head. Maintaining balance depends on - vestibular receptors, vision, proprioceptive receptors in joints and tendons.
64
Describe the anatomy of the peripheral vestibular system?
Vestibular receptors in utricle and saccule and semicircular canals. Vestibular nerve is CN VIII.
65
Describe the anatomy of the central vestibular system
Central vestibular system made up of: vestibular nuclei, caudal cerebellar peduncle, fastigial nucleus of the cerebellum flocculonodular lobe of cerebellum.
66
What are the clinical signs of vestibular disease?
Head tilt,
Nystagmus: involuntary rhythmic oscillation of the eyes - pendular or jerk n, physiologic nystagmus (oculovestiular response), horizontal, fast phase in the direction of the movement. A pathologic nystagmus can be resting nystagmus or positional nystagmus - horizontal, rotatory, vertical. The fast phase is away from the side of the lesion. Vestibular ataxia - falling, rolling, staggering, tight circles towards the side of the lesion, decreased extensor tone ipsilateral limbs, increased extensor tone in contralateral limbs, vomiting and nausea - acute vestibular disease, projections to the emetic centre within the medullary reticular formation, ventral or ventrolateral strabismus, cranial nerve deficits, horners syndrome, hemiparesis and conscious proprioceptive deficits
67
How can you differentiate peripheral vs central vestibular disease?
Central vestibular disease - conscious proprioceptive deficits, vertical resting or positional nystagmus, nystagmus changing direction with changes in head position, cranial nerve deficits other than CN VII, cerebellar signs, decreased level of conscioussness, paradoxical vestibular syndrome.
68
What is paradoxical vestibular syndrome?
Contradictory vestibular signs caused by loss of cerebellar inhibition of the vestibular output.
69
What are the clinical signs of bilateral vestibular disease?
Absent physiologic and or pathologic nystagmus, absent head tilt, side to side swaying of the head, broad based stance, falling to either side,
70
What diagnostic procedures can be used for vestibular disease?
Physical, neurological, otoscopic and pharyngeal examination. haematology and biochemistry, skull radiographs, CT scan or MRI, ear cytology, ear culture and sensitivity, myringotomy, CSF analysis, infectious diseases titers on serum and or CSF, biopsy/histopathology,
71
Describe the anomalous causes of peripheral vestibular disease
Bilateral congenital vestibular disease seen in akitas, beagles.
Congenital peripheral vestibular disease in GSDs, dobermans, english cocker spaniel, siamese cat, burmese cat.
72
Describe the metabolic causes of peripheral vestibular disease?
Hypothyroidism - associated with various neurological signs from seizures to mega esophagus, ,laryngeal and facial nerve paralysis. Mucinous deposits in and around facial and vestibular nerve may cause compression of the axons as they pass through the internal acoustic meatus of the temporal bone.
73
What are the neoplastic causes of Peripheral vestibular disease?
Squamous cell carcinoma (cat, ceruminous gland adenoma (dog and adenocarcinoma (cat), papillary adenoma (dog), lymphosarcoma, osteosarcoma, chondrosarcoma, fibrosarcoma.
74
How may iatrogenic vestibular disease be caused?
Chlorhexidine, aminoglycosides.
Streptomycin and gentamycin > vestibular receptors.
Neomycin, kanamycin and amikacin > auditory receptors.
75
What are the infectious & inflammatory causes of peripheral vestibular disease?
Infectious: otitis media interna,
| inflammatory polyps.
76
What is idiopathic canine geriatric vestibular disease?
It is acute, idiopathic, peripheral vestibular disease which causes vomiting, nausea and severe vestibular deficits. Spontaneous improvement in 3-2 days. Usually normal in 7-10 days in some cases up to 2-3 weeks and sometimes there is a residual head tilt. recurrence is possible. No treatment.
77
What are the causes of central vestibular disease?
Denegerative: inherited lysosomal storage diseases
Anomalous - arachnoid cyst, cerebellar cyst, hydrocephalus
Neoplastic - primary: meningioma, choroid plexus tumour, ependymoma, nerve sheath tumour, glioma. Secondary : lymphosarcoma, hemaengiosarcoma, prostatic or mammary carcinoma. nutritional:thiamine deficiency. Iatrogenic: traumatic cisternal spinal tap.
78
Name the infectious organisms that can cause central vestibular infectious diseases?
Viruses - rabies, pseudorabies, CDV, parvovirus, parainfluenza, herpes. Protozoa - toxoplasmosis, neosporosis
Rickettsia - RMSF, ehrlichia canis
Fungi - cryptococcos, blastomycosis, histoplasmosis, coccidiomycosis, aspergillosis.
Parasites - cuterebra, coenurus, cystercerus, dilofileria immitis, nematodes. Bacteria - pastuerella sp, s aureus, s. epidermis, l monocytogenes. Spirochetes - leptospirosis.
Other - protothecosis.
79
What is granulomatous meningoencephalomyelitis? (GME)
Sunacute to chronic sterile inflammation, suspected immune mediate ddisorder. Female middle age small breed dogs. Disseminated focal and ocular (optic neuritis) form. Prognosis guarded to poor. Definitive diagnosis: histopathology. Traditional treatment: immunosuppresive doses of corticosteroids. Prologned survival time with other immunosuppresive agents in addition to prednisolone such as cytarabine, cyclosporine, procarbazine.
80
What are the toxic causes of central vestibular disease?
Characterised by anorexia, vestibular ataxia and vertical nystagmus. Recovery may be enhanced by administration of diazepam for 3 days. Diazepam competitively displacing metronidazole from GABA receptors. Lead poisoning also can cause toxic central vestibular disease.
81
Describe disease of Cranial Nerve I - olfactory nerve
Loss of appetite, anosmia, nasal discharge, nasal obstruction. DD - viral, bacterial or fungal rhinitis, nasal adenocarcinoma, meningioma, neuroestesioblastoma.
82
Describe disease of cranial nerve II - optic nerve
1. Neuroepithelial cells rods & cons, bipolar and ganglion cells, 2. optic nerve, 3. optic chiasm, 4. optic tract. Lesion: Blindness and PLR deficit.
5. Lateral geniculate nucleus, 6. optic radiation. 7. occipital lobe. Lesion: blindness.
7a. Pretectal nuclei. 8. Edinger-westphal nucles. 9. CN III- oculomotor nerve. 10. ciliary ganglion. 11. ciliary nerves. 12. sphincter pupillae muscle. Lesion: mydriasis, lack of response to light stimulus.
83
Which cranial nerves to the Blindness tests and PLRS evaluate?
Menace response - CN III, complete visual pathway to occipital cortex and CN VII.
Blinking reflex - CN V and VII
Obstacle course/cotton ball test - CN II
PLR - CN II, complete PLR pathway to CN III and sympathetic innervation
Opthalmoscopic exam - retina and CN II
84
What are the DDx for blindness without PLRS?
Bilateral hypoplasia of the optic nerve in dog and cat and horse. Pituitary macroadenoma, miningioma, lymphosarcoma, Vitamin A deficiency in young growing cattle with stenosis of optic canals. Optic neuritis with GME, CDV, Toxoplasmosis, cryptococcosis, blastomycosis, bacterial infections, FIP. Traumatic: craniofacial trauma. vascular: feline ischaemic encephalopathy (optic tracts)..
85
What are the DDx for blindness with INTACT PLRS?
Degenerative: storage diseases
Anomalous: obstructive hydrocephalus, hydranencephaly in ruminants. Primary and metastatic tumours. Polyencephalomalacia in cattle and sheep secondary to thiamine deficiency. Infectious/inflammatory: CDV, TME in cattle, Parasitig migrations. Toxic: lead poisoning. Traumatic head trauma, vascular: cerebral iscahemia following prolonged seizures, anaesthetic accident.
86
Describe disease of cranial nerve III - oculommotor?
Occulomotor nuclei is in midbrain. CN III innervates the dorsal, medial and ventral recti and ventral oblique extraocular muscles. The levator palpebrae muscle of the upper eyelid. Sphincter pupillae muscle for constriction of pupil. So signs are > ventrolateral strabismus, ptosis, mydriasis, no response to light, vision preserved.
87
What is anisocoria?
Unequal pupil size. Lack of sympathetic or parsympathetic. Horners syndrome - miosis, ptosis, enopthalmus, protrusion of the third eyelid.
loss of Parasympathetic - mydriasis, ptosis, ventrolateral strabismus. DDx - sympathetic injury without other neurological deficits: idiopathic, infectious (otitis media), neoplastic (thyroid adenocarcinoma, lypmhosarcoma, nerve sheath tumour), traumatic (dog bite, jugular venipuncture, post op complication). Parasympathetic injury: idiopathic (feline dysautonomia) neoplastic (nerve sheath tumour, meningioma), traumatic (head trauma).
88
Describe disease of cranial nerve IV - trochlear?
Motor - innervates the dorsal oblique extraocular muscle. CN IV deficit: lateral rotation of the eye. Opthalmoscopic exam for animals with round pupil will reveal tilting of the dorsal retinal vein.
89
Describe disease of the cranial nerve IV - trochlear?
Motor - innervates the dorsal oblique extraocular muscle. CN IV deficit: lateral rotation of the eye. Opthalmoscopic exam for animals with round pupil will reveal tilting of the dorsal retinal vein.
90
Describe disease of cranial nerve VI - abducens
Motor - innervates the lateral rectus extraocular muscle and the retractor bulbi muscle. CN VI deficit - medial strabismus, inability to retract the globe. Corneal reflex - opthalmic branch CN V, CN VI and VIII.
91
Describe Cranial nerve V - trigeminal nerve
Mandibular branch - motor - muscles of mastication
Sensory - lower jaw
Opthalmic branch - sensory - dorsal eyelid and cornea
Maxillary branch - sensory - ventral eyelid and nasal area. Assess with palpebral reflex, corneal reflex, pinch upper lip and chin, nasal stimulation, open jaw, observe/palpate skull to detect atrophy of masticatory msucles.
92
What would bilateral and unilateral lesions of the mandibular branch of trigeminal nerve show?
Bilateral - dropped jaw, symmetric atrophy of masticatory muscles, decreased sensation on chin.
unilateral - asymmetry masticatory muscles (atrophy) + decreased sensation on chin.
Opthalmic and maxillary bracnh: ipsilateral sensory deficits.
Diminished behaviour response to facial stimulation may also indicate a lesion to the contralateral somato sensory cortex.
93
What infectious/inflammatory causes can effect cranial nerve V - trigeminal
Rabies and other infectious diseases. Idiopathic trigeminal neuritis - acute bilateral paralysis of the masticatory muscles, doggs and cats, dropped jaw, drooling saliva, difficulty prehending food and drinking, sometimes with horners syndrome, treatment - supportive care, resolution within 2-3 weeks.
94
Which tumours can affect the trigeminal nerve ? CN V
- trigeminal nerve sheath tumour - Unilateral atrophy of masticatory muscles with or without sensory deficits.
Lymphosarcoma - predilection for infiltrating the roots of the cranial nerves.
95
What are the functions of cranial nerve VII? (facial)
Motor - muscles facial expression
Sensory - inner surface pinna
taste sensation rostral two thirds tongue
parasympathetic function to lacrimal gland, nasal glands, mandibular and sublingual salivary glands. Clinical signs of facial nerve diseasE: facial asymmetry, absent movements ear, eyelids, upper lip nostrils, drooling saliva, exposure keratitis, no taste rostral part tongue. May be affected by otitis media, idioppathic facial nerve paralysis, hypothyroidism, polyneuropathy, neoplasms of CN VII or medulla.
96
What are the signs of cranial nerve VIII disease? (vestibulocochlear)
Deafness, otoscopic examination. DD - degeneration auditory receptors/ossicles, congenital deafness, otitis media interna, ototoxic compounds, trauma,
97
What are the functions of cranial nerve IX - glossopharyngeal?
Motor - muscles of parynx.
Sensory - pharyngeal mucosa and caudal third of tongue
Parasympathetic function - zygomatic and parotid salivary glands.
Gag and swallowing reflex, dysphagia - clinical sign.
98
What is the function of cranial nerve X - vagus?
Motor - msucles pharynx, larynx (recurrent laryngeal nervE) and palate. (clinical sign - dysphagia)
Motor parasympathetic - viscera in chest and cranial abdomen (inspiratory dyspnea due to laryngeal paralysis)
Sensory - pharynx, larynx and viscera (megaoesophagus)
99
What are the DDx for CN IX and X deficits
Degenerative storage diseases, congenital hereditary laryngeal paralysis, hypothyroidism, brainstem tumours, paraneoplastic polyneuropathies, idiopathic laryngeal described in middle aged to older male large breed dogs - geriatric onset laryngeal paralysis polyneuropathy, toxic: elad and organophosphate toxicity.
100
Describe The functions of cranial nerve XI (accessory)
Motor - neck muscles (trapeius, sternocephalicus, braciocephalicus) atrophy of neck muscles on palpation. Differential diagnosis - trauma.
101
What are the functions of cranial nerve XII - hypoglossal?
Motor - intrinsic and extrinsic muscles of the tongue. Deficits in tongue movements, atrophy and deviation of the tongue.
102
What are the functions of the cerebellum?
Coordinates all the motor activitieS: voluntary movements, postural movements, reflex movements. Assists in the maintenance of the equilibrium. Controls Rate, Range and Force of movement.
103
What are the clinical signs of cerebellar disease?
Cerebellar ataxia: motor ataxia with strength preserved - broad based stance, titubation: swaying of the body (truncal ataxia) from side to side, forward and backward and occasionally dorsoventrally. Dysmetria : hypo or hypermetria, intention tremors, Vestibular signs and paradoxical vestibular disease, absent menace (ipsilateral), increased muscle tone, normal to exaggerated spinal reflexes, postural reactions are usually normal but increased muscle tone and dysmetria may cause a slight delay. Mild anisocoria, slow PLR, partial third eyelid protrusion and enlarged palpebral fissure (rarE). Decerebellate posture.
104
what are the diagnostic procedures for cerebellar disease?
Physiological and neurological exmaination, MDB, Ct scan or MRI brain, CSF analysis, infectious disease titers on serum and or CSF, biopsy.
105
Which dogs are predisposed to cerebellar abioptrophy?
kerry blue terrier, gordon setter, brittany spaniel, australian kelpie, rough coated collie, beagle, lab, staffie, cats: Siamese, DSH.
106
Describe cortical cerebellar degeneration in american staffordshire terriers?
Onset of neurologic deficits varied from 18 months to 9 years. time from onset of clinical signs to euthanasia: 6 months to 6.5 years. 102 hydroxyglutaric aciduria in this breed can appear in similar manner.
107
Describe degenerative diseases of the cerebellum?
Storage diseases: krabbe's disease or globoid cell leukodystropy, GM1 - gangliosidosis, Gaucher's disease, Sphingomyelinosis, mannosidosis.
Neuroaxonal dystrophy (NAD) - DSH, rottweiler, other breeds.
108
Which conditions can cause cerebellar hypoplasia/aplasia caused in utero by viral infections, genetic disorders or toxins?
Feline panleucopaenia, canine herpes virus, canine parvovirus, BVD, akabane, blue tongue, hog cholera.
109
Which neoplasias can affect the cerebellum?
Primary: medulloblastoma, meningiomas, choroid plexus tumours, ependymomas, nerve sheath tumours, gliomas, lymphosarcomas, steosarcomas, chondrosarcomas, secondary: lymphosarcoma, hemangiosarcoma etc.
110
Which infectious or inflammatory diseases can affect the cerebellum?
Viral, abcterial, protozoal, rickettsial, fungal, parasitic.
Inflammatory - granuloomatous meningoencephalomyelitis (GME), shaker dog disease or corticosteroid responsive tremor syndrome. Shaker dog/corticosteroid responsive - young dogs <5yo, small breeds, mild non suppurative encephalitis, suspected autoimmune mediated etiology, treatment with immunosuppresive doses of corticosteroids tapered over 3-6 months. prognosis - good - 80% of dogs improve within 3-7 days treatment.
111
Which toxic substances can cause cerebellar disease?
Metronidazole intoxication, lead poisoning, penitrem A (mycotoxin), hexachlorphene, metaldehyde, bromethalin, OP.
Traumatic, vascular - infarction.
112
Describe the motor unit
It is a combination of a single motor neurone and all the muscle fibres it innervates. Made up of the soma, peripheral nerve, neuromuscular junction, muscle.
113
What are the clinical signs of lower motor neuron dysfunction
paresis, Depressed tone and reflexes, focal muscle atrophy,
114
Describe peripheral nerve trauma?
Radial nerve common
PNS Trauma - usually unilateral. usually have muscle atrophy and areflexia in innervated muscle. A lot of cases of radial nerve paresis have brachial plexus lesions. Also consider - brachial plexus neuritis, peripheral nerve sheath tumours. Diagnostic aids for trauma: radiography, electromyography, nerve conduction velocities, nerve and muscle biopsy, prognosis: improvement should be seen in 6-12 weeks. full recovery can take > 6 months.
115
What is trigeminal neuritis?
Idiopathic, bilateral, nonsuppurative inflammation of al motor branches of CN V. Present with dropped jaw, r/o Fx. Most recover spontanouesly in 2-3 weeks. Support nutrition while the neuritis resolves.
116
What is polyradiculoneuritis?
An inflammatory condition primarily involving multiple nerve roots. sudden onset of paresis, paralysis, or tetraplegia. Some appear to be hyperaesthetic. Cranial nerve involvement may be prominent. May be a relapsing clinical course. Give general nursing care > corticosteroids usually ineffective. more common in North America in coonhounds.
117
What is diabetic neuropathy?
Dying back neuropathy and schwann cell defects. aetiology incompletely understood. sometimes symmetric pelvic limb LMN paresis. Hyper & hypo adrenocortico id neuropathy also described. Cats have dropped hocks and walk on the hock.
118
What is botulism?
The botulism toxin binds on nerve terminal > internalised onto the vesicle. botulinum toxin: remains at neuromuscular junction > prevents acetylcholine exocytosis. Tetanus toxin: retrograde transport to cNS > internalised by inhibitory interneuron > inhibits release of glycine and GABA.
119
What is myasthenia gravis?
There are congenital and acquired forms, may be pre and pst synaptic. Congenital > presynaptic, synaptic or postsynaptic defects in neuromuscular transmission. Tx: acetylcholinesterase drugs may be of benefit but rarely long term. Acquired: auto immune disease usually affects adult dogs and usually is associated with serum antibodies to nicotinic acetylcholine receptors. Sometimes associated with thymoma. many ultimately go into spontaneous remission. Focal, generalised and acute fulminating fors. Exercise related appendicular muscle weakness, megoesophagus, laryngeal/pharyngeal muscle weakness. Diagnose with anticholinesterase challenge test - tensilon. Anti- ACHr antibody serology. No myopathic or neuropathic changes in muscle and nerve biopsies. Rule out botulism, neuropathies, myoathies. Manage with Rx anticholinesterase (pyridostigmine bromide) or immunosuppressants (prednisolone) take care for aspiration pneumonia. some cases spontaneously improve.
120
What is polymyositis?
Unknown aetiology. must rule out infectious agents. Biopsy. Rx immunosuppressive corticosteroids. follow curse with muscle enzymes.
121
What is masseter myositis?
affects only the Temporal and masseter muscles. Rx biopsy and serum type IIM antibodiies. Rx immunosuppresive corticosteroids.
122
What is dermatomyositis?
Seen in collie dogs, with facial dermatitis and mild generalised myositis, poor response to treatment.
123
What is infectious myositis?
Autoimmune and infectious causes such as toxoplasma neospora and others. Diagnosis with muscle biopsy. treat with clindamycin - follow course with muscle enzymes.
124
What is muscular dystrophy?
Will present with spectacular muscle enzyme elevations. Check EMG changes, muscle biopsy. invariably progressive. An inherited progressive and non inflammatory degenerative muscular disease caused by a Deficency of dystrophin a muscle membrane protein. seen in young dogs.
125
How would a C1-C5 lesion present?
Ataxia with intact reflexes present in all 4 limbs
126
How would a lesion in C6-T2 present?
Same dog with decreased in pelvic thoracic limbs, present in pelvic limbs
127
How would a lesion T3-L3 present?
Thoracic limbs normal, pelvic limbs ataxia with intact reflexes
128
How would a LS intumescence lesion present?
Thoracic limbs normal, reflexes decreased in pelvic limbs.
129
How would a diffuse LMN lesion present?
Reflexes absent in all four limbs
130
Describe the structure of the intervertebral disc?
Annulus fibrosis - fibrocartilage
| Nucleus pulposus - collagenous protein, non collagenous protein, proteoglycan, glycoproteins.
131
Describe the Hansen classification for intervertebral discs
Hansen Type I - extrusion, chondrodystrophic breeds, young (3-6 years), disk in these dogs > cartilage
Increased risk of rupture of annulus & herniation of nucleus pulposus into vertebral canal.
Hansen Type II protrusion only. non chondrodystrophic breeds. Older dogs. fibrous degeneration.
132
What is type I disk disease?
Fibrous IVD gradually > cartilage than fibrous tissue > increased the risk of rupture of annulus fibrosus > herniation of the nucleus pulposus into the vertebral canal.
133
What is the grading of spinal lesions
```
I - spinal pain
II - paraparesis
III paraplegia
IV paraplegia + incontinence
V loss of coonscious perception of pain
```
134
What is the conservative management options for spinal disk disease?
Strict cage rest, analgesia, physiotherapy, nursing, bladder control
135
What are the decompressive surgical options for IVDD?
1. Fenestration
2. Laminectomy
3. Hemilaminectomy
4. Ventral Slot
136
What is the prognosis for IVDD?
Paralysed and no pain perception - about 50% to walk again
Paralysed but feels pain in pelvic limbs - about 80% chance of walking again but could take days, weeks or months.
Rate of onset: fast brutal impact on the cord by disc material causes rapid onset of signs and so has potential to cause myelomalacia.
137
What is fibrocartilagenous embolism?
Sudden onset, mostly non chondrodysplastic dogs, non painful, non progressive, source of cartilage unknown. Dx - exclusion/post mortem. Tx - conservative.
138
What is meningitis arteritis?
More common in young large breed dogs and commonly beagles. sudden onset extreme pain, commonly obtunded, pyrexic. Suppurative leptomeningitis/arteritis. Most dogs respond well to high dose steroids. Bacterial meningitis uncommon in small animals.
139
What is discospondylitis?
Common in young to middle age dogs
Pain > plegia
Infection of the intervertebral disc space
140
What is lumbrosacral malarticulation & malformation?
Classic history of pain on rising or jumping. Mature/middle aged dogs. Signs localisable to L-s Compression. Dx:radiographic /advanced imaging. EMG to outline nerve roots affected. Tx: only Sx successful in logn term.
141
What is degenerative myelopathy?
GSD
> 5 Years of age
Progressive paraparesis, tetraplegia, widespread demyelination of s/c, most severe in T-L region. no treatment, prognosis poor.
142
What is wobblers syndrome? (cervical malformation /malarticulation)
Developmental bone disorder of large breed dogs and horses. young dogs:vertebral formation stenosis of cranial cervical verteebrae. Older dogs:chronic mal articulation of caudal cervical vertebrae, esp doberman pinschers. most often protrusion of annulus fibrosis, sometimes proliferation of articular processes.
143
What is atlantoaxial subluxation?
Common in toy breeds <1 year. traumatic incidents. causes cervical pain, tetraparesis/plegia, sudden death, fracture/separation/absence of the dens. rupture/stretching of atlantoaxial ligaments. Absence of transverse ligament of atlas.
144
Describe spinal cord tumours
Extradural: primary and metastatic vertebral and soft tissue tumours
Intradural/extramedullary: meningiomas & malignant peripheral nerve sheath tumours.
Intramedullary: gliomas and intramedullary metastases.
145
Name the common feline spinal cord diseases
FIP, lymphosaroma, IVDD, ischaemic neuromyopathy, hypervitaminosis A.
146
Describe degenerative intervertebral disc disease
The nucleus pulposus is the inner component, gelatinous in young normal animals. Annulus fibrosus, is the outer layer, ventral portion is thicker than the dorsal. There is no disc at C1-2. The intercapital ligament is from T2 - to T10 which Covers annulus dorsally. Prevents Disc protrusion. Disc degeneration can be a process of aging, dehydration or necrosis and degeneration.
147
Describe hansen type I IVDD?
Type 1 - cartilaginous degeneration in chondrodystrophic breeds. Predisposes to acute extrusion.
148
Describe hansen type II IVDD?
Fibrous degeneration, in older larger breeds, predisposes to chronic protrusion.
149
Describe the pathogenesis of IVDD?
Severity of neurological deficits depends on the amount of disc material extruded, the rate of extrusion, duration of compression.
Chondrodystrophic breeds - dachund, beagle, pekingese, Lhasa apso, cocker spaniel - 3-6 years.
Other breeds - usually older than 6 years of age.
150
What is the most common site of lesion in IVDD?
Most frequent from T11-12 through L3-4, especially T12-13 and T13-L1.
C2-3 in the cervical spine of s mall breeds
C5-6 and C6-7 in Large breeds
Rare in mid thoracic area due to presence of intercapital ligament.
151
What are the clinical signs of IVDD?
pain, ataxia and ambulatory paresis, non ambulatory paresis, paralysis (complete loss of voluntary movements), paralysis with loss of pain perception, descending ascending myelomalacia.
152
What are the clinical signs of cervical disk IVDD?
Pain, reduced movements of the neck and low carriage of the head. Thoracic limb lameness - root signature. Tetra-paresis and ataxia. Tetraplegia. respiratory arrest.
153
What are the clinical signs of thoracolumbar IVDD?
Pain reluctance to move), kyphosis, pelvic limb lameness = root signature, paraparesis and ataxia, paraplegia, loss of sensation and bladder function.
154
How can you localise the lesion of IVDD?
Localise lesion based on neurological examination - pain, cutaneous trunci reflex, muscle tone, spinal reflexes, UMN bladder (distended, easy to palpate but difficult to express, overflow incontinence). LMN bladder - (Flaccid, easy to express but difficult to palpatE). MRI gold standard, myelography, CT or a combination, radiography, haematology, biochemistry and analysis of urine may be inticated in some cases.
155
What is the non surgical treatment for intervertebral disc disease?
Indications - pain, mild neurological deficits, chronic neurological deficits. Exercise restriction first and foremost. Analgesics - discuss risks of analgesia if strict rest is not implemented. Monitor urination and defecation. Nursing care and rehabilitation excercise.
156
What are the indications for surgical intervertebral disc disease treatment?
Significant neurological deficits, pain or mild neurological deficits unresponsive to rest and analgesia. Frequent recurrence of pain or neurological deficits.
157
What are the different surgical treatments for IVDD?
Thoracolumbar - Hemilaminectomy, fenestration
Cervical spine - ventral slot
Lumbosacral space - doorsal laminectomy.
158
What is the prognosis for IVDD?
Pain to paralysis with preservation of sensation - 80-90% success rate. Progressive myelomalacia in 1% of the case with deep pain and 10% without deep pain. Depends also on duration of clinical signs and results of advanced imaging.
Paralysis and loss of deep pain - approximately 50% is surgery performed within 24 hours of loss of deep pain.
159
What is phthisis bulbi?
Severe intraocular pathology (caused by glaucoma, severe uveitis, penetrating or blunt trauma) can lead to a small opaque and end stage eye where ciliary body formation of aqueous has ceased. the degree of corneal opacity usually prevents examination of intraocular tissues. the eye is usually painless by this stage and may be left untreated if this is the case, otherwise enucleate.
160
What is micropthalmos?
A congenitally small eye, often associated with other congenital abnormalities e.g persistent pupillary membranes, corneal opacities, nuclear cataracts, nystagmus, retinal dyspplasia. No treatment. in breeding animals seek the opinion of a clinical familiar with hereditary eye disease.
161
Describe a prolapse of the globe
Prolapse of the globe beyond the plane of the eyelids usually follows known trauma, although this can be quite minot in brachycephalic breeds with naturally prominent globes. the cornea should be kept moist while any life threatening injure are dealt with. the owner can institute this immediately by applying something moist to the corneal surface and gentle pressure with wet cotton wool. Replacement of the globe should be performed under general anaesthesia. The lids should be sutured together for 14 days. Prognosis guarded - optic nerve Vth nerve and medial rectus muscle are frequently damaged.
162
What is bupthalmos?
Also known as hydropthalmos and megaglobus - refers to the globe enlargement that results from chronic glaucoma. Should not be confused with exopthalmos - globe is not particularly prominent when viewed from above, there is no third eyelid protrusion and there will b e intraocular signs of glaucoma. Usually blind, unsightly, painful and prone to exposure problems.
163
Describe the pathology and behaviour of brain tumours
Often divided into extra axial or intra axial based on anatomical site as described by imaging. Extra axial includes meningiomas, schwanomommas, choroiod plexus tumour, intra axial includes gliomes, ependyomomas. Other tumours - intra cranial extension of skull tumours (osteoma/sarcoma, chondrosarcoma) or caudally from nasal chamber. Pituitary based tumours (adenomas, adenocarcinomas) may mushroom into the hypothalamic region. In cats meningiomas predominate, lymphoma and gliomas uncommon. In dogs - meningiomas and gliomas equal. Young individuals may be affected by embryonal tumours e.g medulloblastoma.
164
Describe the pathogenesis of brain tumours
Pathological effects of brain tumours can be divided into primary and secondary effects. Primary effects caused by direct compression and invasion of brain tissue. Secondary effects include adjacent vasogenic oedema, CSF flow disturbance. meningiomas in dogs are superficially invasive, in cats they tend not to be. Gliomas are invasive and destructive.
165
What is the usual clinical presentation of a brain tumour?
often vague and progressive, may be months. May progress/deteriorate acutely. character changes (mimicking old age), vacant walking/circling, standing in corners, seizures developing in middle to old age warrant imaging investigation, cranial nerve deficits, lateralised central neurological deficits, the clinical signs of brain tumours are also site dependent.
166
What are the ddx for brain tumours?
Meningitis, hepatic encephalopathy, GME, distemper, other focal brain diseases; abscesses, GME
167
Which diagnostic investigations/ are done for brain tumours?
CBC and biochemistry to rule out metabolic causes. Chest radiographs as part of routine health assessment. Advanced i maging - MRI and CT - extra axial - broad based + surface contact (dural tail), mild mass effect and oedema, variable enhancement, Pituitary based - mushrooming from pituitary fossa, usually homogenous enhancement but sometimes cystic and heterogenous. Csf sampling - beware sudden alteration in CSF dynamics following cisternal pressure may cause cerebellar herniation and acute medullary compression leading to respiratory arrest. hyperventilation under anaesthesia may reduce ICP by reducing CSF pressure secondary to reduced PcO2. CSF may be altered but non specific often.
168
What palliative therapy may be used for brain tumours?
Anti epileptic drugs as appropriate
Corticosteroids - dexamethasone 0.25mg/kg Intravenously
If comatosed: intubate and hyperventilate to reduce pCO2 and thereby reduce intra cranial pressure.
169
Is surgery effective for for brain tumours?
Surgery - specialist surgical procedure, requiring specialist anaesthesia support and peri operative intensive care. May be curative for meningiomas in cats especially on more accessible convex surfaces of cerebrum. Unlikely to be curative for canine meningiomas and gliomas due to the invasive nature of tumours. Cytoreductive surgery may be beneficial prior to radiation therapy.
170
How Is radiation therapy used for brain tumours?
Fractionated and coarse fractionated protocols are described as sole therapy with similar response rates and survival tiems. Coarse fractionated protocols have potentially more side effects eg ischaemic necrosis but reported less than 10%. Adjuvant radiation following surgery gives better Survival times especially for meningiomas.
171
How is chemotherapy used for brain tumours?
Blood brain barrier limits the brain penetration by most drugs. No chemotherapy proven. Anecdotal reports of lomustine (CCNU), carmustine (BiCNU) and hydroxyurea.
172
Describe the pathology and behaviour of spinal cord tumours
Classified on histology and on anatomical basis. intramedullary tumours are rare in dogs and cats. intradural extramedullary tumours account for 35%; meningiomas, peripheral nerve sheath tumours. Extradural tumours account for up to 50% - primary bone tumours of vertebrae, metastatic involvement of vertebra. Compression of cord is common to all types of spinal cord tumours.
173
what is the usual clinical presentation of spinal cord tumours?
Often vague and slowly progressive over a few months. Intra medullary tumours are more rapid - few weeks. Ischaemia and haemorrhagic events will give acute deterioration. Progressive pain and paresis, acute paralysis.
174
Which diagnostic investigations should be done in spinal cord tumours?
Neurological evaluation to localise where possible. Survey radiographs of vertebral column. CSF may contain lymphoblasts associated with lymphoma. CT and MRI are most useful imaging techniques. Surgical exploration and biopsy. Prognosis poor as treatment options are limited. euthanasia due to uncontrollable pain or paraplegia may be best option.
175
What are the possible treatments for spinal cord tumours?
Intra operative cytology may identify lymphoma, extradural malignant tumours may be cyto reduced but rarely cured, intradural extramedullary tumours in particular meningioma can sometimes be completely removed, involvement of the cord limits any attempts for wide excision. Radiation therapy - spinal cord is prone to radiation induced ischaemic damage and therefore radiation therapy is rarely performed. Solitary lymphoma or solitary plasmacytoma of vertebrae can be responsive to radiation at non toxic doses. Chemotherapy for lymphoma standard protocols can be used.
176
Describe the pathology and behaviour or peripheral nerve sheath tumours
Tumours arise from peri axonal schwann cells = schwannomas, tumours arising from peri neural fibroblasts - neurofibroma/sarcoma. Brachial plexus is most Common site in dogs. Extension proximally into spinal canal is common. Other tumours can affect brachial plexus e.g lymphoma.
177
What is the typical clinical presentation of a peripheral nerve sheath tumour?
Often vague and slowly progressive, present with variable lameness with no defined focus. Paresis and muscle atrophy in later stages, pain on passive manipulation of limb, pin on deep palpation into axilla. Edge of mass may be palpable in deep axilla. Prognosis poor. euthanasia due to uncontrollable pain may be best option.
178
What are the possible treatments for peripheral nerve sheath tumours?
involvement proximally into spinal canal limits opportunity for wide excision. the spinal cord is prone to radiation induced Ischaemic damage and therefore rarely performed. following Cytoreductive surgery anthracycline based protocols have been suggested but with unproven benefit.
179
Describe tumours of the eye
Ocular tumours may involve eyelids, third eyelid and conjunctiva, globe, orbit and optic nerve. Benign tumours of the eyelids are common in dogs. Squamous cell carcinoma of the eyelid in white faced cats are associated with UV light exposure. Clinical presentation > mass on lid, ulcerative erosive lesion, rarely metastasise.
180
What are the treatments for eyelid tumours?
Small tumours removed by wedge shaped Excisional biopsy. Large tumours require wide excision with flaps to reconstruct. Large excisions may result in non functional lids requiring enucleation. Strontium-90 pleisiotherapy for superficial squamous cell carcinoma and mast cell tumours of lids may be effective. No proven chemotherapy. Benign and early malignant tumours carry fair to good prognosis with adequate local treatment. Large invasive malignant tumours have high local recurrence rate unless wide excision plus enucleation is performed.
181
Describe the pathology and behaviour of tumours of the globe?
Generally uncommon. Intra ocular sarcoma of cats associated with previous ocular trauma. Limal melanoma - essentially benign. Melanoma arising from iris or ciliary body. dogs - locally invasive but low metastatic rate. Cats - locally invasive and high metastatic rate. Ciliary body adenocarcinoma more common in dog than cat. locally invasive but low metastatic rate. Intraocular sarcoma of cats - locally invasive and high metastatic rate. Metastatic tumours (osteosarcoma), lymphoma as part of multicentric lymphoma.
182
What is the clinical presentation of tumours of the globe? What diagnostic investigations would you do?
Conjunctivitis, obvious mass bulging from globe or distorting iris and pupil, secondary uveitis and glaucoma.
Investigate - opthalmic examination, chest radiographs, ultrasound of the globe, MRI, FNA especially of regional lymph nodes.
183
What is the prognosis for tumours of the globe?
Canine intra ocular tumours carry a good prognosis folowing enucleation. feline intraocular tumours carry a guarded prognosis following enucleation. feline intraocular sarcomas carry a poor prognosis due to high metastatic rate. Intra occular lymphoma is a poor prognostic factor for multicentric lymphoma. Limbal melanoma may be treated by local excision and adjucant sr-90 radiation.
184
Describe the pathology and behaviour of tumours of the orbit and optic nerve
Various tumour types may expand into/invade the retrobulbar space. eg osteosarcoma of bones of orbit, maxillary sarcomas, intranasal malignant tumours, intranasal lyphoma. Or meningioma arising from the optic nerve sheath. Clinical presentations ; exopthalmos, protrusion of third eyelid, deviation of eye, unable to retropulse eye, loss of vision/ligth reflexes, pain (more common with abscess).
185
What diagnostic investigations and staging should be done for orbit/optic nerve tumours? what is the prognosis?
Radiographs, ultrasound, CT or MRI imaging, ultrasound guided FNA or core biopsy <80% definitive diagnosis. FNA useful to differentiate tumour from abscess. Prognosis; bone invasive and limited options for wide excision give poor prognosis.
186
What are the treatment options available for tumours of the optic nerve/Orbit?
Orbit exenteration is treatment of choice. Adjuvant radiotherapy following surgery may improve local control. Primary radiotherapy may be useful in cats to control intra nasal lymphoma with extension intro retrobulbar space. Lymphoma invading retrobulbar space can be treated with standard protocols. Metastases are rare for most tumour types, local recurrence is common.
187
Describe the different breathing patterns that may be seen with head trauma?
Cheyne-stokes respiration: periods of hyperventilation which taper off gradually to periods of apnea of variable duration. when respiration resumes gradually accelerates to the point of hyperventilation. lesion in deep cerebral hemispheric structures, basal ganglia and diencephalon. central neurogenic hyperventilation: at approximately 25 breaths per minute. Apneustic breathing: cycles of prolonged inspiration expiration and apnea, every cycle lasts approximately for a minute. also cluster breathing followed by periods of apnea. Lesion in caudal pons and medulla. Ataxic or gasping respirations (agonal rbeathing) lesion in medullary respiratory centres.
188
List your DDx for seizures
Distemper, FIp, FIV, FeLV, toxoplasma, neopspora, cryptococcus, rabies, primary or met neopasia, GME, SRME, trauma, thromboembolism, hypertension, hydrocephalus, hepatic encephalopathy, uraemia, hyperkalaemia, hypocalcaemia, hypoxia, hyperparathryoidism, hypoglycaemia, hyperthermia, acid base imbalance, toxins: lead, organophosphates, metaldehyde, strhychnine. Treat with in dogs; phenobarbital and potassium bromide (potentially dizepam). in cats - diazepam and potassium bromide.
189
List 5 infectious agents of the CNS and for each give the name of the resulting neurological disease
Canine distemper virus - CNS signs may occur weeks or months after recovery - cause myoclonus, rhythmic brief sudden contractions of muscle groups, also seizures, ataxia, vestibular disease. Rabies - acute onset of behavioural changes with aggression or dumb form, dumb form characterised by lesions in the brainstem nuclei leading to dropped jaw and ptyalism. FIP - non effusive form may only cause CNS signs such as seizures. In utero infection with feline panleucopeniia virus can cause cerebellar hypoplasia - ataxia and wide base stance for life. FIV - neurological signs may be seen due to meningoencephalitis but signs can be vague or include only mild behavioural changes
190
What are the clinical signs of cerebellar disease?
Cerebellar ataxia - characterized by failure of motor coordination, broad base stance hypermetria and titubation. Titubation - swaying of the body and head from side to side, forward and backward, dysmetria - the cerebellum controls the rate range and force of movement. Cerebellar disease can be associated with hypometria or hypermetria but hypermetria is far more common. hypermetria can be observed in all four limbs but is usually more evident in the front limbs as a spastic high stepping gait. intention tremors - head and neck tremors that appear after the initiation of a movement and become more severe when the animal is getting closer to the target, tremors of the eyeballs could produce a pendular nystagmus. Typical signs of vestibular disease: lloss of balance, nystagmus, strabismus, head tilts can be associated with a lesion of the vestibulocerebellum, fastigial nucleus and caudal cerebellar peduncles, lesions of the flocculonodular lobe and caudal cerebellar peduncles cause paradoxical vestibular disease. absent menace response with normal vision & facial nerve. Increased muscle tone and normal to exaggerated spinal reflex. delayed postural reactions in a pure cerebellar lesion conscious proprioception is always intact but the response can be delayed or exaggerated due to the increased muscle tone and dysmetria. aniscoria - ipsilateral or contralateral pupilary dilation and slowly responsive to light. Decerebellate posture.
191
How can you differentiate decerebellate posture and decerebrate posture?
by the animals level of conscioussness, that should be normal in a lesion of the cerebellum and severely impaired in decerebrate animals. (opisthotonus and hypertonus of all four limbs)
192
Describe the treatment of Status epilepticus
Stop seizure with diazepam IV or per rectum, repeat up to three times, if still seizuring, use propofol, d not administer rapidly, place IV catheter, AB, check for obstruction, administer oxygen, monitor body temp, check blood glucose, PCV, total solids and BUN. Start IV fluids, prevent other seizure by starting a constant rate infusion of diazepam or phenobarbital or propofol CRI.
193
What are the clinical signs that may be seen in a cat with chronic total radial nerve paralysis?
Non weight bearing, knuckling, decreased reflexes, tone, and muscle atrophy of the thoracic limb extensor muscles, lameness, exercise intolerance, poor grooming, ataxia and increase tone and reflexes in pelvic limbs.
194
What are the common infectious agents recognised to cause neurological disease in the dog and cat ? what diagnostic tests are available to assist diagnosis and what therapeutic approach would you take
FIP, FIV, FELV, distemper, rabies, parvo, herpes viruus, Rocky Mountain spotted fever, leptospirosis, cryptococcus, aspergillosis, toxoplasma. Distemper - respiratory signs, oculonasal discharge, pleural effusion, bronchial changes, cutaneous hyperkeratosis of nasal planum and pads, Vomiting and diarrhoea, Seizures, ataxia and meningioencephalitis, myoclonus. Serology, ELISA and CSF analysis to detect disease. treat symptomatically. just give steroids for inflammatory conditions, antibiotics when necessary, anti emetics, fluid therapy for dehydration, decongestants for nasal discharge, thoracocensis for effusions, diazepam for seizures.
195
List four cranial nerves, their functions and the reflexes/ responses used for their evaluation in the neurological examination
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Optic nerve (11): vision - menace response; PLR.
Oculomotor (II)- extra ocular motor control and pupillary dilation/constriction, PLR and eyemovement. Trigeminal nerve (V): facial sensation and muscles of mastication, palpebral reflex, mastication, muscle tone. Facial nerve (VII): facial expression muscles and little sensory on pinnae of ear, palpebral reflex, and muscle tne.
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196
What is cheyne stokes respiration?
Periods of hyperventilation which taper off gradually to periods of apnea of variable duration. when respiration resumes gradually accelerates to the point of hyperventilation. caused by a lesion in deep cerebral hemispheric strucutes, basal ganglia and diencephalon.
197
What is central neurogenic hyperventilation?
at approx 25 breaths per minute. lesion in caudal mesencephalon and poons.
198
What is apneustic breathing?
cycles of prolonged inspiration, expiration and apnea, every cycle lasts approximateely for a minute. also cluster breathing followed by periods of apnea. Lesion in caudal pons or medulla
199
What is ataxic or gasping respirations (agonal breathing)
Lesion in medullary respiratory centres
200
What is your plan when the presenting problem = seizures?
History - state of consciousness, posture and movements, presence of autonomic signs such as salivation, defecation and urination, duration of seizure, events before seizure and between seizures, exposure to toxicants, previous trauma? DDX - hydrocephalus, hepatic encephalopathy, neoplasia, infectious diseases such as CDV, idiopathic, traumatic, toxicity, vascular. Perform bile acids stim test to check if liver disease. Brain MRI. IE - first seizure normally 1-5 years. REgular periods between seizures and some may present as cluster seizure. Treat with phenobarbitone.
