Neurology AI Flashcards
1
Q
How can abnormal eye movement be observed if the vestibular system is challenged?
A
By changing the head position or putting the patient on its back.
2
Q
What is the purpose of testing corneal sensation?
A
To assess the response to touching the cornea and observe globe retraction and/or blink.
3
Q
Which cranial nerves are involved in corneal sensation?
A
CN V (afferent pathway) and CN II and CN VI (efferent pathways).
4
Q
How can the response to stimulation of the nasal mucosa be evaluated?
A
By touching the nasal mucosa and observing withdrawal of the head.
5
Q
What cranial nerves are involved in the response to stimulation of the nasal mucosa?
A
CN V (afferent pathway) and a response.
6
Q
What is the purpose of testing jaw tone?
A
To assess the resistance of the jaw to opening the mouth.
7
Q
How can tongue movement be assessed?
A
By observing tongue movement and symmetry.
8
Q
Which cranial nerve is responsible for tongue movement?
A
CN XII
9
Q
How can gagging and swallowing be evaluated?
A
By offering food or stimulating the hyoid bone externally.
10
Q
Which cranial nerves are involved in gagging and swallowing?
A
CN IX, X, XI
11
Q
Why is evaluating the olfactory nerve challenging?
A
Because it remains subjective and not commonly performed.
12
Q
What additional information may be required to evaluate the olfactory nerve?
A
A history of anorexia and other neurological signs.
13
Q
How is the list of differential diagnoses formulated?
A
Based on signalment, onset, progression, and response to therapy.
14
Q
What are the possible categories for differential diagnoses (excluding VITAMIND and DAMNITV)?
A
Vascular, Inflammatory, Trauma/toxin, Anomalous, Metabolic, Idiopathic, Neoplastic/nutritional, Degenerative.
15
Q
What are the different localizations for neurological abnormalities?
A
Intracranial (forebrain, brainstem, and cerebellar), spinal (C1-C5, C6-T2, T3-L3, L4-S2), and neuromuscular.
16
Q
What does a forebrain syndrome include?
A
Cerebrum (cerebrocortical grey matter, cerebral white matter, and basal nuclei) and diencephalon.
17
Q
What is the main function of the cerebral cortex?
A
Behavior, vision, hearing, fine motor activity, and conscious perception of touch, pain, temperature, and body position.
18
Q
What is the main function of the cerebral white matter?
A
Conveying motor and sensory function instructions.
19
Q
What is the main function of the basal nuclei?
A
Muscle tone and initiation/control of voluntary motor activity.
20
Q
What is the main function of the diencephalon?
A
Sensory integration, control of autonomic and endocrine function, sleep, consciousness, olfactory functions, vision, and pupillary light reflex.
21
Q
What are the possible neurological examination findings in a forebrain syndrome?
A
Altered mentation/changes in behavior, possible contralateral lack/decreased menace, normal gait and possible abnormal posture, possible contralateral deficits in posture, normal to increased contralateral muscle tone, facial and body contralateral absent to decreased sensation, seizures/hemi-neglect syndrome, cervical hyperaesthesia, rarely movement disorders.
22
Q
What is the function of the cerebellum?
A
To regulate and coordinate motor activity, maintain equilibrium, and preserve normal body position at rest or in motion.
23
Q
What are the possible neurological examination findings in a cerebellar syndrome?
A
Ipsilateral menace deficits, vestibular signs/anisocoria, intention tremors/hypermetria, ataxia/broad base stance, delayed initiation/exaggerated proprioception, normal to increased spinal reflexes/ upper motor neuron (UMN) muscle tone.
24
Q
What are the clinical signs of proprioceptive ataxia?
A
Loss of awareness of limb position in space.
25
What are the clinical signs of vestibular ataxia?
Head tilt and a tendency to lean, drift, fall, or roll to one side.
26
What are the clinical signs of cerebellar ataxia?
Abnormal 'uncontrolled' limb movements and hypermetria.
27
What is the difference between paresis and plegia?
Paresis is weakness or inability to generate movement voluntarily, while plegia is complete loss of voluntary movement.
28
What is the difference between tetraparesis/plegia and hemiparesis/plegia?
Tetraparesis/plegia affects all four limbs, while hemiparesis/plegia affects one side of the body.
29
What is the difference between paraparesis/plegia and monoparesis/plegia?
Paraparesis/plegia affects the hind limbs, while monoparesis/plegia affects only one limb.
30
What are the criteria for LMN paresis?
Difficulty supporting weight, short strides, flaccid motor function, decreased segmental reflexes, and decreased resting muscle tone.
31
What are the criteria for UMN paresis?
Abnormal limb position, stiff and ataxic gait, delayed protraction collapse, spastic motor function, normal to increased segmental reflexes, and normal to increased resting muscle tone.
32
What is proprioception?
Awareness of the position and movement of the head, body, and limbs.
33
Where are the proprioceptive receptors located?
In the joints, tendons, muscles, and inner ear.
34
What tests can be used for proprioceptive testing?
Paw positioning, hopping, placing and visual placing, wheelbarrowing, extensor postural thrust, hemiwalking, and paper sliding tests.
35
Which postural reaction test is commonly used in dogs for proprioceptive positioning?
Paw positioning.
36
How is the paw positioning test evaluated?
By turning the paw over and determining how quickly the animal corrects the position.
37
Why is it important to support the animal's weight during the paw positioning test?
To improve test sensitivity and ensure the animal is standing firmly on all four limbs.
38
What is the purpose of segmental spinal reflexes?
To help localize the lesion further into different spinal cord segments and monitor disease progression.
39
What makes up the peripheral nervous system?
12 pairs of cranial nerves and 36 pairs of spinal nerves.
40
What do peripheral nerves contain?
Motor and sensory axons.
41
Where do motor axons extend from?
Neurons located in the ventral horn of the spinal cord or the grey matter of the brainstem.
42
Where do sensory axons have their cell body?
In the dorsal root ganglion or in homologous ganglia of cranial nerves.
43
How do most spinal nerves leave the vertebral canal?
Through the intervertebral foramina formed between pedicles of adjacent vertebrae.
44
What reflex can be performed to evaluate cervical intumescence and brachial plexus nerves?
Withdrawal reflex.
45
What reflexes can be performed on the pelvic limbs?
Not mentioned in the course notes.
46
Why is neuroanatomical localisation important in formulating differential diagnoses?
To prevent inappropriate diagnostic tests and costly experiences.
47
How can the neurological examination be divided?
Into six sections: mentation, gait evaluation, postural reaction testing, segmental spinal reflexes, evaluation of pain and sensation, cranial nerve examination.
48
Is there a specific order to follow during the neurological examination?
No, but it's best to establish a routine to avoid missing any section.
49
What are the different classifications of mental status?
Normal, disorientated, drowsy/obtunded, stuporous, comatose.
50
What are some abnormal behaviors that can accompany altered mental status?
Aggression, compulsive walking, loss of learned behavior, head pressing, stargazing, hemi-neglect syndrome.
51
What can altered mental status be caused by?
Intracranial pathology or metabolic abnormalities such as hypoglycemia, hepatic or uraemic encephalopathy.
52
How many different postures should be differentiated?
Three different postures: Schiff-Sherrington, decerebrate rigidity, decerebellate rigidity.
53
What is the difference between Schiff-Sherrington posture and the other two?
Schiff-Sherrington is related to spinal injury, while the other two are related to brain pathology.
54
What is decerebrate rigidity characterized by?
Extension and increased tone in all four limbs with extension of the head and neck.
55
What is decerebellate rigidity characterized by?
Increased extensor tone in the thoracic limbs, flexed pelvic limbs, and extension of the neck and head.
56
What is the aim of gait evaluation?
To identify affected limbs and classify changes as incoordination, weakness, or lameness.
57
What other abnormalities can be observed during gait evaluation?
Leaning, falling, or circling tendencies can be seen.
58
Where should gait evaluation be performed?
In a place where the animal can walk freely, ideally on a non-slippery surface.
59
What is ataxia?
Lack of coordination that can arise from peripheral nerve or spinal cord lesions.
60
What are the two types of ataxia?
Proprioceptive or sensory ataxia, and vestibular ataxia.
61
What are the clinical signs caused by cerebellar lesions?
Altered mental status, variably affected cranial nerves, tetra/hemi paresis/plegia, affected proprioception, normal to increased muscle tone, possible cervical hyperaesthesia, cardiac/respiratory abnormalities.
62
What are the functions of the brainstem?
Regulatory centers for consciousness, cardiovascular system, and breathing; links cerebral cortex to spinal cord through ascending and descending motor pathways; contains 10 pairs of cranial nerves (III to XII).
63
What are the clinical signs caused by brainstem lesions?
Altered mental status, possibly abnormal cranial nerves, tetra/hemi paresis/plegia, affected proprioception, normal to increased muscle tone, possible cervical hyperaesthesia, cardiac/respiratory abnormalities.
64
What is the vestibular system responsible for?
Maintaining balance and normal orientation relative to gravitational field of the earth; maintaining position of eyes, neck, trunk, and limbs relative to head movement.
65
What are the clinical signs of central vestibular syndrome?
Head tilt (ipsilateral/contralateral), spontaneous horizontal/vertical/rotatory nystagmus, variable positional reaction, possibly abnormal mental status.
66
What are the clinical signs of peripheral vestibular syndrome?
Ipsilateral head tilt, horizontal/rotatory nystagmus, normal positional reaction, normal mental status.
67
What is the structure of the spinal cord?
Central grey matter with sensory neurons, interneurons, and lower motor neurons; peripheral white matter divided into dorsal, lateral, and ventral funiculi.
68
How many spinal cord segments are there in dogs and cats?
8 cervical, 13 thoracic, 7 lumbar, 3 sacral, and at least 2 caudal; not all correspond to vertebral bodies.
69
What is the difference between upper motor neurons and lower motor neurons?
Lower motor neurons are efferent neurons connecting CNS to somatic or visceral muscle; upper motor neurons control and influence lower motor neurons.
70
What are the clinical signs of lower motor neuron dysfunction?
Flaccid paresis/paralysis, decreased to absent muscle tone, decreased to absent segmental reflexes, rapid and severe neurogenic muscle atrophy.
71
What are the clinical signs of upper motor neuron dysfunction?
Spastic paresis/paralysis, normal to increased muscle tone, normal to increased segmental reflexes, late and mild disuse muscle atrophy.
72
What is the motor unit composed of?
The motor unit is composed of the LMN, neuromuscular junction, and muscle fibers.
73
What are muscle fibers composed of?
Muscle fibers are composed of several hundred myofibrils containing myofilaments.
74
What is the difference in motor units between muscles responsible for fine movements and muscles responsible for coarse movement?
Muscles responsible for fine movements have small motor units, while muscles responsible for coarse movement have large motor units.
75
What are the possible neurological examination findings for mental status?
The possible neurological examination findings for mental status are normal.
76
Which cranial nerves may show abnormalities in the neurological examination?
Possible abnormalities can be found in cranial nerves VII, IX, and X.
77
What are the possible posture/gait findings in the neurological examination?
Possible findings include flaccid tetraparesis/plegia in posture/gait.
78
What deficits can be observed in proprioception on affected limbs?
Deficits may be observed on affected limbs in proprioception.
79
What can be observed in spinal reflexes and muscle tone in affected limbs?
Spinal reflexes and muscle tone may be decreased to absent in affected limbs.
80
What can be observed in sensation during the neurological examination?
Sensation can be normal or decreased to absent in nociception and sensation.
81
What other findings can be observed during the neurological examination?
Other findings that may be observed include self-mutilation.
82
What are the clinical signs caused by neuromuscular lesions?
Clinical signs caused by neuromuscular lesions are variable and depend on the pathology.
83
What references can be consulted for further information?
References include BSAVA Manual of Canine and Feline Neurology 4th Edition and Handbook of Veterinary Neurology 4th Edition.
84
Why is information regarding species, age, breed, sex, and coat color important in history taking?
Some conditions have a predilection for certain species, age groups, breeds, and coat colors.
85
Why is it important to know the animal's background in history taking?
To identify any previous health conditions or concurrent/systemic problems that may contribute to the neurological signs.
86
What specific questions should be asked to establish the onset and progression of the condition?
Questions about the nature of onset (acute, insidious, chronic) and progression (improvement, deterioration, wax and waning, paroxysmal).
87
What terms can be used to describe gait abnormalities?
Weak, wobbly, or lame.
88
What terms can be used to describe paroxysmal episodes?
Seizure, loss of balance, or collapse.
89
Why is a thorough physical examination important in neurology?
To identify systemic diseases and concurrent problems that may present with neurological signs.
90
What is the aim of the neurological examination?
To establish the nature of the condition and the neuroanatomical localisation.
91
What is the next step after establishing the neuroanatomical localisation?
Formulating a differential diagnosis list.
92
What does the withdrawal reflex evaluate?
The lumbar intumescence, femoral and sciatic nerves.
93
What does the patellar reflex evaluate?
The L4-L6 spinal cord segments and femoral nerve.
94
What does the perineal reflex evaluate?
The S1 to Cd5 and pudendal nerve.
95
How is the cutaneous trunci reflex performed?
By pinching the skin between T2 and L4-L5.
96
What muscles contract during the cutaneous trunci reflex?
The cutaneous trunci muscles bilaterally.
97
In what cases can the cutaneous trunci reflex be lost ipsilaterally?
In cases of caudal brachial plexus lesions.
98
What is the significance of a lack of a cutaneous trunci reflex?
It has no significance in the absence of other neurological deficits.
99
What should be tested last during spinal palpation?
The area suspected to be painful.
100
What is evaluated by conscious response to a painful stimulus?
Nociception.
101
Why is the evaluation of nociception important?
It assesses the severity of a lesion and its prognosis.
102
What is the purpose of cranial nerve examination?
To localize intracranial conditions and assess peripheral nerve diseases.
103
What is the first stage of cranial nerve examination?
Assessment of symmetry.
104
What are the structures assessed for symmetry in cranial nerve examination?
Masticatory muscles (CN V), ears and lips (CN VII), pupil size (CN II and III), eye position (CN III, IV, and VI), palpebral fissure (CN III or V), and third eyelid (sympathetic nerve or CN V).
105
How can vision be evaluated in cranial nerve examination?
By leaving the animal to navigate in new surroundings or blindfolding each eye.
106
How is the palpebral reflex performed?
By touching the medial and lateral canthus of the eyes.
107
What does the pupillary light reflex involve?
Shining a light in the eyes to cause pupillary constriction.
108
What is assessed by the menace response?
Blinking in response to a menacing gesture.
109
When can physiological nystagmus be elicited?
By moving the head from side to side and up and down.
110
When is pathological nystagmus usually seen?
At rest in cases of pathology.
111
What are the different directions of pathological nystagmus?
Vertical, horizontal, and rotatory.
112
What can sometimes make assessing the cutaneous trunci reflex difficult?
Overweight patients.
113
What are the three divisions of neuromuscular diseases?
The three divisions are peripheral nerve, neuromuscular junction, and muscular pathology.
114
How many pairs of cranial nerves are there in the peripheral nervous system?
There are 12 pairs of cranial nerves in the peripheral nervous system.
115
Where are the motor axons located in the nervous system?
Motor axons are located in the ventral horn of the spinal cord or grey matter of the brainstem.
116
Where are the sensory axons located in the nervous system?
Sensory axons have their cell bodies in the dorsal root ganglion or homologous ganglia of cranial nerves.
117
What are the components of the neuromuscular junction?
The components are axon terminal, synaptic cleft, and endplate region of a skeletal muscle fiber.
118
What is the function of the neuromuscular junction?
The neuromuscular junction converts electrical signals to chemical signals and back to electrical signals.
119
What happens when an action potential reaches the nerve terminal?
The action potential depolarizes the axon, causing calcium channels to open and acetylcholine vesicles to be released.
120
What is the role of acetylcholine in the neuromuscular junction?
Acetylcholine binds to receptors in the endplate region of skeletal muscle fibers, triggering muscle contraction.
121
What is the main function of skeletal muscles?
Skeletal muscles function to maintain body posture.
122
What order is function lost in progressive spinal cord diseases?
The order is proprioception, motor function, bladder function, and nociception.
123
What are the most important factors for pet owners when it comes to epilepsy treatment?
Drug efficacy and possible side effects.
124
What is the lifelong commitment required when starting epilepsy medication for pets?
Regular administration and in some cases regular monitoring.
125
When can the maintenance dose of potassium bromide be started?
After the five loading dose days.
126
What can be done if the seizures cease before the five days loading is completed?
Start the maintenance dose to try to minimize the side effects.
127
What is levetiracetam thought to act by modifying?
Calcium-dependent exocytosis of neurotransmitters.
128
What does levetiracetam bind to?
SV2A pre-synaptic vesicular system.
129
When is levetiracetam generally used?
As an add-on drug.
130
When can levetiracetam be used as a first choice?
In certain cases such as in patients with compromised liver function.
131
What is the loading dose of levetiracetam?
60-90 mg/kg IV once.
132
When should a blood sample be taken for exclusion of metabolic and toxic causes?
At the time of presentation.
133
What should be measured prior to increasing the dose of an anti-epileptic drug?
Serum levels of the drug.
134
When should blood tests be repeated?
A few days after initial presentation.
135
What should be done if seizures are seen occasionally?
Diazepam or midazolam can be used.
136
What should be considered if despite drug loading or inability to control further seizures?
A constant rate infusion drug.
137
How long should a constant rate infusion be maintained?
At least six hours.
138
How should the dose of diazepam be reduced?
By 50% every 6 hours to avoid withdrawal seizures.
139
What are the dose and administration requirements for midazolam?
0.2mg/Kg bolus followed by 0.2-0.3mg/Kg/hour in saline.
140
What is the recommended bolus dose of propofol?
1-2mg/Kg to effect.
141
What is the definition of status epilepticus?
Continuous seizure activity for longer than 30 minutes or repeat episodes without return to normality within 30 minutes.
142
What is the definition of cluster seizures?
Two or more seizures within a 24-hour period.
143
What is the aim of emergency seizure treatment?
To either stop the episode itself or prevent any further seizures from happening.
144
What can be the consequences of status epilepticus and cluster seizures?
Permanent brain damage or even death, and a higher chance of euthanasia.
145
What is the aim of immediate control during emergency treatment?
To stop seizure activity and avoid systemic effects.
146
What is the function of diazepam in immediate control of seizures?
Increases the inhibitory post-synaptic potential, increasing seizure threshold and inhibiting seizure spread.
147
What is the dose of diazepam for immediate control?
Bolus of 0.5 to 2mg/Kg IV up to 20mg or 1 to 2mg/Kg rectally.
148
What is the function of midazolam in immediate control of seizures?
Acts as a benzodiazepine alternative to diazepam.
149
How is midazolam administered for immediate control?
Bolus of 0.2mg/Kg IV or 0.2mg/Kg intranasally.
150
What is the recommended dose for midazolam CRI during immediate control?
0.3mg/Kg/hour.
151
What are the systemic effects that need to be controlled during emergency seizure treatment?
Airway, breathing, circulation, and vital parameters.
152
Why is monitoring of vital parameters important during emergency seizure treatment?
To monitor heart rate, respiratory rate, peripheral pulses, temperature, and avoid complications.
153
What is the primary aim of anti-epileptic drug therapy during emergency treatment?
To stop seizure activity and prevent further seizures.
154
What is the loading drug of choice for patients not currently on medication and with no known liver pathology?
Phenobarbitone.
155
What is the loading dose of Phenobarbitone?
18-24mg/Kg within 24 hours (18mg/Kg in cats).
156
What is the loading protocol for severe cases of status epilepticus?
Initial dose of 12mg/Kg IV followed by two to three injections of 3-4mg/Kg.
157
What are the side effects of zonisamide in dogs?
The side effects of zonisamide in dogs include sedation, decreased appetite, vomiting, and behavioral changes.
158
How is zonisamide metabolized in the body?
Zonisamide is metabolized in the liver by hepatic microsomal enzymes.
159
What is the recommended dose of zonisamide for dogs?
The recommended dose of zonisamide for dogs is 5-10 mg/kg twice daily.
160
What is the mode of action of zonisamide?
The mode of action of zonisamide is unknown.
161
What is the recommended dose of gabapentin for seizure management?
The recommended dose of gabapentin for seizure management is 10-20 mg/kg TID.
162
What is the most common side effect of gabapentin?
The most common side effects of gabapentin are sedation and ataxia.
163
What is the half-life of zonisamide in dogs?
The half-life of zonisamide in dogs is three to four hours.
164
What are the possible side effects of zonisamide?
The possible side effects of zonisamide include ataxia, sedation, vomiting, hepatopathy, renal tubular acidosis, and dry eye.
165
What are the side effects of gabapentin?
The side effects of gabapentin include sedation and ataxia.
166
Why is zonisamide not widely used in veterinary medicine?
Zonisamide is not widely used in veterinary medicine due to its high cost.
167
What is the recommended dosing frequency for zonisamide in dogs?
Zonisamide should be given two times daily.
168
What is the recommended dose of zonisamide in refractory cases?
The recommended dose of zonisamide in refractory cases is 10 mg/kg BID or a 25% reduction in phenobarbitone dose.
169
How is gabapentin excreted from the body?
Gabapentin is nearly exclusively excreted via the kidneys.
170
What are the reported side effects of zonisamide in dogs?
The reported side effects of zonisamide in dogs include sedation, decreased appetite, vomiting, and behavioral changes.
171
What is the recommended dose of zonisamide for dogs already on phenobarbitone?
The recommended dose of zonisamide for dogs already on phenobarbitone is 10 mg/kg BID.
172
What is the recommended dose of zonisamide for pulse therapy in cluster seizures?
The recommended dose of zonisamide for pulse therapy in cluster seizures is 60-90 mg/kg followed by 20-30 mg/kg given three to four times daily until no seizures are seen for 24 hours.
173
What are the essential elements of monitoring and supportive care for patients with epilepsy?
Urinary catheter placement, turning, eye and mouth care.
174
What are some factors that can contribute to treatment failure in epilepsy?
Genetic factors, poor owner compliance, drug discontinuation, inadequate blood levels, inadequate therapy, drug interaction/malabsorption, development of a new condition, incorrect diagnosis.
175
How can drug discontinuation be avoided in epilepsy treatment?
By assessing owners' lifestyle and explaining the consequences associated with drug discontinuation.
176
What can be responsible for breakthrough in seizure control in epilepsy?
Hepatic induction associated with phenobarbitone administration, increase salt uptake and increase bromide clearance in dogs swimming in the sea.
177
Why is correct identification of a seizure important in epilepsy treatment?
Incorrect therapy can be initiated with no change in the frequency/severity of the events.
178
What are some recommended references for further reading on epilepsy treatment?
Bateman SW, Parent JM, Charalambous M, Bhatti SFM, Van Ham L, Platt S, Jeffery ND, Tipold A, Siedenburg J, Volk HA, Hasegawa D, Gallucci A, Gandini G, Musteata M, Ives E, Vanhaesebrouck AE, Hardy BT, Patterson EE, Cloyd JM, Moore SA, Munana KR, Papich MG, Platt SR, Randell SC, Scott KC, Chrisman CL, Hill RC, Gronwall RR, Haag M, Podell M, Smeak D, Lord LK, Wagner SO, Sams RA, Zimmermann R, Hülsmeyer V, Gindiciosi B, Palus V, Eminaga S, Villiers E, Bruto Cherubini G, Peters RK, Schubert T, Clemmons R, Vickroy.
179
What are the recommended monitoring intervals for phenobarbitone therapy?
10-15 days, 45 days, 90 days, 180 days, every six months to yearly thereafter
180
How should dose adjustments be made for phenobarbitone therapy?
Based on serum levels, not oral dose
181
In which cases is potassium bromide indicated?
Low initial seizure frequency or liver disease
182
What are the possible side effects of potassium bromide?
Polyphagia, polyuria, polydipsia, ataxia, weakness, and pancreatitis
183
How should potassium bromide be administered?
With food to avoid gastrointestinal signs
184
What should be done in case of suspected potassium bromide overdose?
Immediately reduce the oral dose and administer 0.9% sodium chloride solution if severe
185
What factors can influence potassium bromide serum levels?
Abrupt dietary changes, exposure to sea water, and certain medications
186
What is the recommended monitoring interval for potassium bromide?
2 months, 4-6 months, and 6 months to yearly thereafter
187
What should be considered when changing food or allowing the patient to swim in the sea?
Possible influence on potassium bromide serum levels
188
What is the recommended starting dose of imepitoin?
10 mg/kg/BID
189
What are the reported side effects of imepitoin?
Polyphagia, hyperactivity, polyuria, polydipsia, and sedation
190
Is serum level monitoring required for imepitoin?
No, it is not required
191
In which cases is the usage of imepitoin contraindicated?
Cases with renal function impairment
192
What is the main excretion route for levetiracetam?
Unchanged in the urine
193
What is pleocytosis?
An increased WBC count in cerebrospinal fluid.
194
How can blood contamination affect CSF interpretation?
It can falsely increase protein level and cell count.
195
What is albuminocytological dissociation?
Increased protein level with normal total cell count.
196
What are the abnormal findings associated with albuminocytological dissociation?
Compressive lesions, neoplasia, ischaemic or degenerative myelopathy.
197
How is lymphocytic pleocytosis characterized?
Increased protein level, >5 WBC/uL with >50% lymphocytes.
198
What conditions can cause lymphocytic pleocytosis?
Lymphoma, necrotizing non-suppurative meningoencephalitis.
199
What is mixed cell pleocytosis?
Increased protein level, >5 WBC/uL, mainly a mixture of lymphocytes and mononuclear cells.
200
What conditions can cause mixed cell pleocytosis?
GME, fungal and protozoal diseases.
201
What is neutrophilic pleocytosis?
Increased protein level, >5 WBC/uL with neutrophilic predominance.
202
What conditions can cause neutrophilic pleocytosis?
Steroid-responsive meningitis-arteritis, bacterial meningitis, following myelography.
203
What is eosinophilic pleocytosis?
Increased protein level, >5 WBC/uL with eosinophilic predominance.
204
What conditions can cause eosinophilic pleocytosis?
Parasitic or idiopathic pathology.
205
What can cytological evaluation of CSF identify?
Cellular inclusions, abnormal lymphocytes, and rarely larvae.
206
What infectious etiologies can be tested using CSF PCR in dogs?
Canine distemper virus, Neospora, Toxoplasma.
207
What infectious etiologies can be tested using CSF PCR in cats?
Toxoplasma, feline coronavirus.
208
When can culture of CSF be performed?
If the history is consistent with an infectious etiology.
209
What does the presence of bacterial intracellular inclusions in CSF suggest?
Bacterial meningitis.
210
What do electrodiagnostic tests assess?
The functional activity of the peripheral nervous system.
211
What are the different types of electrodiagnostic tests?
Electromyography, nerve conduction velocity, repetitive nerve stimulation.
212
What is the purpose of muscle and nerve biopsies?
To aid in the diagnosis of a suspected neuromuscular disease.
213
What tests can aid in the diagnosis of certain neuromuscular pathologies?
CK activity, titres to Type IIM antibodies, Neospora Caninum, Toxoplasma.
214
When are muscle and nerve biopsies typically performed?
When a diagnosis has not yet been reached for a suspected neuromuscular disease.
215
What percentage of epileptic dogs are controlled with anticonvulsant medication?
70%
216
How are refractory cases of epilepsy defined?
Less than 50% reduction in seizure frequency with a certain medication
217
What is the aim of the treatment for epilepsy in dogs?
Seizure control, not a cure
218
What are the possible outcomes of successful treatment for severe cases of epilepsy?
Reduction of seizure length, increased period between episodes, change in pattern
219
When should medication not be swapped for a well-controlled patient?
If there are no major side effects
220
What is the initial goal of treating any dog with epilepsy?
Monotherapy to reduce drug-drug interactions and adverse effects
221
When should anti-epileptic drug therapy be started?
If there are two or more seizures within a six-month period; if status epilepticus or cluster seizures occur; or if post-ictal signs are severe or last longer than 24 hours
222
What is the first line drug of choice for the management of seizures in dogs?
Phenobarbitone
223
When are steady state concentrations of phenobarbitone reached after initiation of therapy?
After seven to 10 days
224
What is phenobarbitone metabolized by?
The liver
225
What are some of the side effects seen soon after initiation of phenobarbitone treatment?
Polyphagia, polyuria, polydipsia, ataxia, and sedation
226
What are the more serious side effects of phenobarbitone treatment?
Blood dyscrasias and hepatotoxicity
227
When are dyscrasias most commonly seen after starting phenobarbitone treatment?
Within the first three months
228
What is the higher risk associated with hepatotoxicity?
Serum levels higher than 35 ug/ml
229
What tests are recommended prior to initiation of phenobarbitone therapy?
Haematology, biochemistry, and bile acid stimulation test
230
What should be regularly monitored during phenobarbitone treatment?
Phenobarbitone serum levels
231
What are the advantages of MRI?
Exquisite soft tissue detail, gold standard for most neurological pathologies
232
What are the disadvantages of MRI?
Expensive, danger due to high magnetic fields, relatively slow image acquisition times
233
What is the limited value of ultrasound in neurology?
Confirmation of hydrocephalus, identifying soft tissue masses (e.g. brachial plexus) or intramedullary lesions intraoperatively
234
In what cases is cerebrospinal fluid analysis useful?
Cases where a CNS inflammatory pathology is suspected
235
Where can cerebrospinal fluid be collected from?
Cisterna magna, lumbar cistern, or both sites depending on neuroanatomical localization
236
When should CSF collection be performed?
After advanced imaging in cases of intracranial pathology, only if there are no signs of increased intracranial pressure
237
What should be checked when collecting CSF for specific tests?
Amount needed for analysis, preservation instructions from the external laboratory
238
What are the characteristics of normal CSF?
Clear and colorless, may be pink to red (hemorrhage), yellow or xanthochromic (old hemorrhage), yellow-green (purulent inflammation or neoplasia), or grey/black (melanin granules or melanocytes)
239
What is the expected protein level in normal dogs from lumbar collections?
<40mg/dL
240
What is the expected total nucleated cell count in normal CSF?
<5WBC/uL, no erythrocytes
241
What does an increased erythrocyte count in CSF indicate?
Hemorrhage
242
What are some advantages of radiography?
Widespread availability, relatively inexpensive, quick to acquire
243
What is radiography good for in assessing the spine?
Good survey technique, assessing bone lesions
244
What are some disadvantages of radiography?
Insensitive for soft tissue pathology, relatively insensitive for detecting bone lysis, challenging to interpret
245
What is myelography used for?
Diagnosis of spinal pathology, investigation of compressive lesion of the spinal cord
246
How is myelography performed?
General anesthesia, survey radiographs, injection of contrast into subarachnoid space, radiographic projections
247
What are some advantages of myelography?
Low cost, quicker assessment of spine than MRI, dynamic studies in suspected instability
248
What are some disadvantages of myelography?
Risks, paresis and ataxia may worsen, contrast reaction, seizures, death, difficulty performing and interpreting
249
Where can the injection of contrast be performed for myelography?
Cisterna magna or L5-L6 or L6-L7 disc space
250
Why should CSF analysis be performed prior to myelography?
Myelography may cause deterioration of clinical signs in cases of inflammatory CNS disease
251
What is the recommended time frame for analyzing CSF collected during myelography?
Within 30-60 minutes to minimize cellular degradation
252
What is the recommended dose of contrast medium for myelography?
0.2 to 0.3ml/Kg
253
What is an important factor in managing seizure patients?
Correct recognition, underlying cause identification, and appropriate treatment.
254
Why may a video be essential in characterizing a seizure?
A good description of the episode is not always possible.
255
What aids in understanding the underlying cause of a seizure?
Thorough history taking and physical and neurological examinations.
256
Is epilepsy a self-limiting condition?
Yes, it can be self-limiting but in most cases, it is lifelong.
257
What is the underlying cause of an epileptic seizure?
Abnormal physio-electrical activity of the brain.
258
How can seizures be classified based on frequency?
Isolated, clustered, or continuous (status epilepticus).
259
What are the two types of seizures based on manifestation?
Focal (partial or automotor) or generalized (tonic-clonic, clonic, atonic, or absence episodes).
260
What is status epilepticus?
Duration above five minutes or several seizures without return to normal mentation in between.
261
What can impaired mentation present as during a focal manifestation?
Automatism, such as aggression episodes or inappropriate vocalization.
262
How can the aetiology of seizures be divided into groups?
Seizures Extracranial, Intracranial Reactive, Secondary Probable Symptomatic, and Idiopathic.
263
What are reactive epileptic seizures?
Transient reaction of the normal brain caused by metabolic disease or intoxication.
264
What are probable symptomatic epileptic seizures?
Suspected underlying but unidentifiable brain disease.
265
What are symptomatic epileptic seizures?
Result from structural forebrain pathology.
266
What is idiopathic epilepsy?
No cause identified and presumed to be genetic in origin.
267
What should be taken for a complete blood count?
A blood sample.
268
What can further blood tests depend on?
Clinical signs and results of the CBC and biochemistry.
269
What are the three different lesion localisations mentioned in the course notes?
Extradural, Intradural/ extramedullary, Intramedullary
270
Which lesion localisation is associated with deviation of the contrast column?
Extradural
271
What is the golf tee sign often seen in?
Intradural/ extramedullary cases
272
Name two examples of lesions associated with Intradural/ extramedullary localisation.
Arachnoid cysts, Meningomas
273
What does spinal cord swelling suggest in the case of an intramedullary pathology?
Divergence of the dorsal and ventral contrast columns
274
Name two examples of intramedullary pathologies.
Glioma, Myelitis
275
What can be considered if the physical examination and blood work-up are normal?
Advanced imaging should be performed.
276
In what situations can computed tomography (CT) be useful?
Identification of skull fractures, detection of acute intracranial haemorrhage, lesions associated with mass effect, or contrast uptaking lesions.
277
What should be performed for cell count and protein concentration measurements?
A cerebellomedullary cerebrospinal fluid collection.
278
When is idiopathic epilepsy diagnosed?
If all the results are negative.
279
What should be given prior to anesthesia in cases of intra-cranial pathology?
Drugs such as mannitol or furosemide.
280
When should CSF collection not be performed?
In cases of suspected intracranial pathology especially prior to an MRI being completed.
281
What are the electrophysiologic indicators of acute canine polyradiculoneuritis?
Fibrillation potentials, positive sharp waves, decreased and dispersed nerve conduction velocities.
282
What is the definitive diagnosis for acute canine polyradiculoneuritis?
Nerve biopsy.
283
How is the treatment for acute canine polyradiculoneuritis determined?
Based on the severity of the clinical signs.
284
What are the clinical signs of aortic thromboembolism in cats?
Paraparesis or paraplegia, weak or absent femoral pulses, pain, pale or cyanotic footpads and nails, and hypothermia of the distal limbs.
285
What can cause ischaemia to muscles and nerves in aortic thromboembolism?
Restriction of blood flow and the release of vasoactive substances.
286
In which animals is aortic thromboembolism usually associated with underlying cardiac disease?
Cats.
287
What is the prognosis for aortic thromboembolism?
Depends on the underlying cause.
288
What is another name for canine neosporosis?
Neospora caninum infection.
289
What are the clinical and neurological characteristics of aortic thromboembolism in dogs?
Clinical signs include loss of nociception, stiff pelvic limbs, and hard and painful muscles.
290
What is the main focus of treatment for acute canine polyradiculoneuritis?
Supportive care.
291
What is the main factor in determining the severity of treatment required for acute canine polyradiculoneuritis?
The severity of the disease.
292
How long does it take for most dogs with acute canine polyradiculoneuritis to fully recover?
A few weeks to up to 6 months, depending on the severity of the disease.
293
What are the electromyographic changes seen in acute canine polyradiculoneuritis?
Fibrillation potentials and positive sharp waves.
294
What is the underlying cause of aortic thromboembolism in cats?
Underlying cardiac disease.
295
What is the main treatment approach for aortic thromboembolism?
Treatment is beyond the scope of this lesson.
296
What should be closely monitored in dogs with severe cases of aortic thromboembolism?
Respiratory depression.
297
What are the clinical signs of acute canine polyradiculoneuritis in more severe cases?
Recumbent patient, intensive nursing, and potential respiratory depression.
298
What condition is characterized by an acute onset of paraparesis or paraplegia in cats?
Aortic thromboembolism.
299
What causes ischaemia to muscles and nerves in aortic thromboembolism?
Restriction of blood flow and release of vasoactive substances.
300
What are some common electrophysiologic indicators of acute canine polyradiculoneuritis?
Fibrillation potentials and positive sharp waves.
301
What are the characteristics of the pelvic limbs in aortic thromboembolism in cats?
Stiff and painful.
302
What is the main focus of treatment for aortic thromboembolism in cats?
Treatment depends on the underlying cause.
303
What is the prognosis for aortic thromboembolism in cats?
Prognosis depends on the underlying cause.
304
What are the clinical signs of acute canine polyradiculoneuritis?
Electromyographic changes, decreased and dispersed nerve conduction velocities.
305
What is the main factor in determining the treatment approach for acute canine polyradiculoneuritis?
Severity of the clinical signs.
306
What is the prognosis for acute canine polyradiculoneuritis?
Most dogs tend to recover fully within a few weeks to up to 6 months.
307
What is the underlying cause of aortic thromboembolism in dogs?
Not mentioned in the course notes.
308
What is the underlying cause of aortic thromboembolism?
Restriction of blood flow and release of vasoactive substances.
309
What is the correlation between the severity of acquired MG and antibody concentration?
There is poor correlation between the severity of the disease and the antibody concentration.
310
What conditions have been associated with acquired MG?
Tumors (thymomas, osteogenic sarcomas) and hypothyroidism.
311
What further investigations are recommended for cases of acquired MG associated with tumors or hypothyroidism?
Imaging of the thorax and abdomen, as well as blood tests.
312
What is the role of electrodiagnostic tests in diagnosing acquired MG?
They can assist diagnosis, but lack sensitivity and specificity.
313
What is the recommended use of neostigmine in acquired MG cases where oral administration is not possible?
It can be administered intravenously, intramuscularly, or subcutaneously upon duration of response, but total dose should not exceed 2mg/Kg/daily.
314
What should be done once oral administration is safe in acquired MG cases?
Pyridostigmine can be started.
315
What is the dose range and administration frequency of pyridostigmine?
The dose range is 0.2-5mg/Kg BID or TID, and should be started low then increased to effect.
316
What are possible side effects of neostigmine and pyridostigmine in acquired MG cases?
Vomiting, increased salivation, diarrhea, and abdominal cramps.
317
How can side effects of neostigmine and pyridostigmine be reversed?
With atropine.
318
When can neostigmine be used to determine if the weakness is a result of overdose or insufficient medication in acquired MG cases?
When it is uncertain, neostigmine can be used.
319
What does the presence of side effects after using neostigmine indicate in acquired MG cases?
It indicates overdosing.
320
What does an improvement with additional neostigmine suggest in acquired MG cases?
It suggests increasing the current medication.
321
What are some supportive care measures for acquired MG?
Elevation of food and water or placement of a percutaneous endoscopic gastrostomy tube.
322
What is the correlation between resolution of clinical signs (including megaoesophagus) and the return of AChR antibody titres to normal range in acquired MG cases?
There has been excellent correlation.
323
When can medication be discontinued in acquired MG cases?
Once ACh receptor antibodies are within the normal reference range and the signs have resolved.
324
What is the prognosis of acquired MG in early stages and fulminant cases?
The prognosis is guarded.
325
What are the possible outcomes if no complications develop and there is a good response to treatment in acquired MG cases?
The prognosis can be good, but relapses are possible.
326
What is idiopathic polyradiculoneuritis?
It is an inflammation of the nerve roots and peripheral nerves.
327
What is the suspected cause of idiopathic polyradiculoneuritis?
An immune-mediated process involving both a humoral and cell-mediated process.
328
What are some common clinical signs of idiopathic polyradiculoneuritis in dogs and cats?
Changes in gait, stiffness, short strided gait, collapsing, and possibly facial nerve deficits and dysphonia.
329
Which nerve roots and components of spinal nerves are mainly affected by idiopathic polyradiculoneuritis?
The ventral nerve roots and ventral root components.
330
What is the usual progression of idiopathic polyradiculoneuritis in terms of limb involvement?
The pelvic limbs are generally affected first, and the condition can progress to affect all four limbs.
331
What can sometimes happen in uncommon situations with idiopathic polyradiculoneuritis?
The opposite can happen, where the condition initially affects all four limbs then progresses to only affect the pelvic limbs.
332
Is discomfort a feature of idiopathic polyradiculoneuritis?
Discomfort is not a feature of the disease, but can sometimes be seen associated with muscles and joints.
333
What is the potential respiratory complication in severe cases of idiopathic polyradiculoneuritis?
Respiratory compromise due to involvement of the intercostal muscles and diaphragm can result in respiratory arrest.
334
How is the diagnosis of idiopathic polyradiculoneuritis made?
Based on the clinical history and clinical findings.
335
What can increased protein levels with normal cell count in CSF analysis indicate in idiopathic polyradiculoneuritis?
A confirmation of the clinical suspicion.
336
What are some tests that can help confirm the diagnosis of idiopathic polyradiculoneuritis?
Electrodiagnostic tests and nerve biopsies.
337
What are the components of a motor unit?
The components of a motor unit are the motoneuron, neuromuscular junction, and myofibers.
338
What are the three variations of motor units?
Motor units can vary in terms of size, histochemical properties of myofibers, and functional properties related to contraction speed and fatigue resistance.
339
Describe the functional anatomy of the neuromuscular junction.
The neuromuscular junction consists of an axon terminal, synaptic cleft, and endplate region of a skeletal muscle fiber.
340
How are electrical signals converted in the neuromuscular junction?
Electrical signals (nerve impulses) are converted to chemical signals (acetylcholine release) and then back to electrical signals (muscle action potentials).
341
What happens when acetylcholine (ACh) is released at the neuromuscular junction?
ACh diffuses across the synaptic cleft and binds to specific ACh-receptor sites on the postsynaptic sarcolemma, increasing permeability to Na+ and K+ ions.
342
What causes local depolarization of the endplate in muscle fibers?
The binding of ACh to its receptors causes a local depolarization of the endplate, generating muscle action potentials across the sarcolemmal surface.
343
What happens after the local depolarization of the endplate?
Opening of Na+ channels and Ca++ channels in the transverse tubules and sarcoplasmic reticulum occurs, leading to myofibril contraction.
344
What is the function of the acetylcholine receptor (AChR)?
The AChR is a nicotinic receptor that binds acetylcholine and initiates muscle fiber depolarization.
345
What does the peripheral nervous system (PNS) consist of?
The PNS consists of 12 pairs of cranial nerves and 36 pairs of spinal nerves.
346
Where do motor axons and sensory axons extend from in the PNS?
Motor axons extend from neurons in the ventral horn of the spinal cord or grey matter of the brainstem, while sensory axons have their cell body in the dorsal root ganglion or cranial nerve ganglia.
347
What is a dermatome?
A cutaneous region innervated by afferent nerve fibers from a single spinal nerve is called a dermatome.
348
What is a myotome?
The musculature innervated by a single spinal nerve is termed a myotome.
349
How are spinal nerves covered and protected?
Spinal nerves are covered by connective tissue (epineurium) and further wrapped in perineurium, with individual nerve fibers surrounded by the endoneurium. Schwann cells create a myelin sheath around myelinated axons.
350
What determines the speed of conduction in nerves?
The speed of conduction depends on axon diameter and myelination, with larger diameter and myelinated axons conducting faster.
351
What is the role of myelin in nerve conduction?
Myelin, produced by Schwann cells, allows saltatory conduction from node to node, increasing the speed of conduction.
352
Can nerves in the peripheral nervous system regenerate?
Yes, nerves in the PNS can regenerate as long as the endoneurial and Schwann cell tube are not completely severed.
353
What happens in a complete transection (neurotmesis) of a nerve?
Regeneration only occurs if the axon can find the distal stump of the nerve.
354
What are partial lesions to a nerve called?
Partial lesions to a nerve are called neuropraxia.
355
What are some factors that can influence nerve conduction?
Toxic, metabolic, and degenerative factors can influence nerve conduction.
356
What is the name of the protein kinase coding gene associated with lysine-deficient in cats?
WNK4
357
What is the primary location of the lysine-deficient 4 protein kinase enzyme?
Distal nephron
358
What is the underlying pathomechanism in affected cats with lysine-deficient 4 protein kinase?
Potassium wasting nephropathy
359
How can the diagnosis of Burmese hypokalaemia be reached?
Via a DNA test
360
What type of disease is Burmese hypokalaemia?
Autosomal recessive
361
Which breeds are at risk of Burmese hypokalaemia?
Asian, Australian Mist, Bombay, Burmilla, Cornish Rex, Devon Rex, Singapura, Sphynx, Tiffanie and Tonkinese
362
What is the usual treatment for hypokalaemia in cats?
Potassium supplementation
363
In severe cases of hypokalaemia, what type of fluid is initially used for potassium supplementation?
Potassium-supplemented intravenous fluids
364
Do cats with periodic hypokalaemic polymyopathy need life-long potassium supplementation?
Not all of them, some may spontaneously improve by the time they reach 1-2 years of age
365
What is the protozoan that causes neosporosis?
Neospora caninum
366
Which animals can be affected by neosporosis?
A wide range of warm-blooded animals, including domestic and wild animals
367
What are the two ways Neospora caninum can be transmitted?
Vertically and horizontally
368
What are the symptoms of neosporosis in puppies?
Progressive paraparesis, muscle atrophy, loss of patellar reflexes, paralysis, and joint deformation
369
What are the neurologic signs in adult dogs with neosporosis?
Multifocal CNS syndrome, paresis, paralysis, hypermetria, anisocoria, delayed proprioception and reflexes, ataxia, head tilt, head tremors, and seizures
370
What are some of the other clinical manifestations of neosporosis in adult dogs?
Myositis, myocarditis, hepatitis, dermatitis, ocular lesions, interstitial pneumonia, and pancreatitis
371
How can neosporosis be diagnosed?
Clinical signs, serology, and other tests depending on the tissues affected
372
What is the focus of neosporosis treatment?
Control of clinical manifestations rather than parasitological cure
373
What are the important factors to consider in investigating peripheral vestibular disease?
The signalment, history (onset and progression), response to medication, and neurological examination.
374
What are some further investigations that can be considered in cases of peripheral vestibular disease?
Otoscopic examination, skull radiographs, tympanic bulla ultrasound, microbiology, myringotomy, fine needle aspirates, biopsies, and serology.
375
When should advanced imaging such as CT or MRI be considered in cases of peripheral vestibular disease?
When reaching a diagnosis either by identifying the problem or by exclusion of differential pathologies.
376
What are the common characteristics of canine idiopathic vestibular disease?
Usually unilateral, acute to peracute onset, head tilt, ataxia, pathological nystagmus, and sometimes changes in mentation.
377
Is there a breed or age predisposition for canine idiopathic vestibular disease?
No, although cases are usually over 5 years old.
378
What is the typical recovery period for canine idiopathic vestibular disease?
Usually within two to three weeks, with gradual improvement over the first 3-5 days.
379
What is the most common cause of peripheral vestibular disease in dogs and cats?
Otitis media/interna.
380
What signs indicate involvement of the inner ear in otitis media/interna?
Vestibular signs, facial nerve deficits, and post ganglionic sympathetic neuron deficits (Horner's syndrome).
381
What are some diagnostic tools for otitis media/interna?
Otoscopic examination, bulla imaging, and sampling.
382
Which imaging modality is often chosen in the work-up of peripheral vestibular cases?
CT (computed tomography) due to lower cost and increased speed of image acquisition.
383
What does MRI (magnetic resonance imaging) have better sensitivity for in evaluating inner ear pathology?
Evaluation of cochlear and vestibulocochlear nerve roots.
384
What is the most common cause of vestibular disease in cats?
Inflammatory polyps.
385
At what age are inflammatory polyps typically seen in cats?
At a young age.
386
What signs may precede other associated signs in cases of inflammatory polyps?
Vestibular signs, respiratory or ear disease.
387
What are some imaging modalities that may be necessary for the diagnosis and treatment planning of inflammatory polyps?
Radiographs, CT (computed tomography), or endoscopy.
388
Can surgery for polyp removal lead to persistent vestibular signs and facial nerve paresis?
Yes.
389
What could radiographs identify in cases of suspected inflammatory polyps?
Soft tissue filling of the tympanic cavity.
390
What are the clinical signs associated with Granulomatous Meningoencephalitis (GME)?
The clinical signs vary depending on the areas affected and can be further classified as multifocal, focal, or ocular forms.
391
How can the final diagnosis of Granulomatous Meningoencephalitis (GME) be achieved?
The final diagnosis can only be achieved by tissue biopsy or post mortem examination.
392
What are the typical lesions described in Granulomatous Meningoencephalitis (GME)?
The lesions are typically described as perivascular cuffs of inflammatory cells in the parenchyma and meninges of the brain and spinal cord.
393
What are the characteristics of the focal form of Granulomatous Meningoencephalitis (GME)?
The neurological signs associated with the focal form generally suggest a single space-occupying lesion that may affect different areas of the brain.
394
Why is the diagnosis of focal GME challenging?
From an imaging point of view, neoplasia or vascular pathologies may be as likely as an inflammatory lesion.
395
What is the most common form of Granulomatous Meningoencephalitis (GME)?
The most common form is the multifocal form, which affects different areas of the central nervous system (CNS).
396
What imaging technique is preferable for identifying lesions in multifocal GME?
MRI is preferable to CT for identification of lesions in multifocal GME.
397
What is the ocular form of GME characterized by?
Ocular GME manifests as acute onset of blindness and is considered an ophthalmologic problem.
398
What were necrotising meningoencephalitis (NME) and necrotising leukoencephalitis (NLE) previously referred to as?
NME was previously called Pug encephalitis, whereas NLE was called necrotising encephalitis of the Yorkshire terriers.
399
What is the clinical onset like in NME and NLE?
The clinical onset is slightly different between NME and NLE.
400
What is the preferable name for necrotising encephalitis when there is no histopathologic confirmation available?
Necrotising encephalitis is a preferable name when there is no histopathologic confirmation available for the respective pathology.
401
When should serology or PCR on CSF be considered?
Serology or PCR on CSF should be considered to exclude infectious causes of meningoencephalitis.
402
What is the primary drug used to treat canine neosporosis?
Clindamycin
403
What is the additional antiprotozoal activity possessed by Clindamycin?
Lincosamide
404
Which drug combination is highly effective against neosporosis?
Clindamycin and sulphonamide
405
How long should the treatment duration be for neosporosis?
Four to 8 weeks
406
What should be done if one littermate is identified with neosporosis?
Test and treat the others if positive
407
What should be avoided in seropositive dogs with neosporosis?
Immunosuppressive drugs
408
What is the disorder resulting from either a deficiency or functional disorder of the nicotinic acetylcholine receptor?
Myasthenia gravis (MG)
409
What are the breeds associated with an autosomal recessive trait for congenital MG?
Jack Russell Terriers, Smooth Fox Terriers, Springer Spaniels
410
What breed has a reversible form of congenital MG?
Smooth Haired Miniature Dachshunds
411
How can the diagnosis of congenital MG be confirmed?
Clinical signs of exercise-induced weakness
412
What type of clinical signs may be seen in acquired MG?
Focal or generalised neuromuscular weakness
413
What are the three clinical syndromes associated with acquired MG?
Focal, generalised, and fulminating
414
What can be used for a presumptive diagnosis of MG?
Neostigmine
415
How can exercise tolerance be assessed in a dog with MG?
Administration of neostigmine and exercise
416
What is the confirmation for the diagnosis of MG?
Presence of circulating ACh receptor antibodies
417
What is the good correlation in acquired MG between the disease course and antibody titres?
The clinical course and the antibody titres
418
When are false negative results in antibody titre possible in acquired MG?
If the patient was on immunosuppressive therapy for longer than 7-10 days
419
In which stage of the disease is a negative antibody titre result possible?
Early stages of the disease
420
What are the components involved in evaluating the motor component of pathological nystagmus?
Oculomotor, trochlear, and abducens cranial nerves.
421
What does pathological nystagmus indicate?
A disruption in the vestibular system components, MLF, or motor nuclei of abducens, trochlear, and oculomotor nerves.
422
How can pathological nystagmus be classified?
Based on the fast phase and direction: vertical, horizontal, or rotatory.
423
In which cases does physiological or pathological nystagmus not occur?
Bilateral vestibular disease, bilateral otitis media/interna, or idiopathic causes.
424
What is vestibular strabismus?
An intermittent abnormal eye position reflecting loss of innervation of the extraocular muscles.
425
What causes the deviating ventral eye position in vestibular strabismus?
Challenging the head position by extending the neck or placing the animal in dorsal recumbency.
426
How do you differentiate between peripheral and central vestibular disease?
Through clinical features, differential diagnoses, investigations, and prognosis.
427
What are the common features of peripheral and central vestibular disease?
Altered mentation, changes in gait, proprioceptive deficits, and cranial nerve involvement.
428
What are reliable findings of central vestibular disease?
Changes in gait, proprioception, and pathological nystagmus with a change in head position.
429
What is paradoxical vestibular disease characterized by?
Head tilt away from the lesion and proprioceptive deficits on the same side as the lesion.
430
What is the specific lesion involved in paradoxical vestibular disease?
Caudal cerebellar peduncle or flocculonodular lobe of the cerebellum on the opposite side of the head tilt.
431
Why is accurate neuroanatomical localization important in differentiating peripheral and central vestibular disease?
To decide which tests to perform and provide a prognosis.
432
What are the different breed related pathologies associated with meningoencephalitis of unknown aetiology?
GME, NME, NLE
433
What is the preferable name for inflammatory CNS disease where a histopathological diagnosis is not available?
Meningoencephalitis of unknown aetiology
434
What is the cause of meningoencephalitis of unknown aetiology?
Exaggerated immune response against the central nervous system, but no trigger identified
435
How is meningoencephalitis of unknown aetiology diagnosed?
Presumptive diagnosis based on signalment, history, MRI features, CSF analysis when available, and exclusion of infectious diseases
436
What are the common clinical signs of vestibular disease?
Mostly intracranial signs with possible spinal cord involvement
437
How can peripheral and central vestibular disease be differentiated?
Based on neurological examination findings
438
What are some possible differential diagnoses for neuromuscular diseases?
Metabolic, neoplasia, toxin exposure, infectious aetiologies
439
What are the recommended tests for investigating meningoencephalitis of unknown aetiology?
Full haematology, biochemistry, urinalysis, thoracic and abdominal imaging
440
Which imaging modality is the advanced imaging of choice for meningoencephalitis of unknown aetiology?
MRI
441
What can be done to reach a presumptive diagnosis in cases of meningoencephalitis of unknown aetiology?
Cerebrospinal fluid analysis including total protein measurement, differential cell count, and cytological evaluation
442
What are some common clinical signs of neuromuscular disease?
Exercise intolerance, weakness, decreased reflexes, decreased muscle tone, severe muscle atrophy.
443
What are some less common clinical signs of neuromuscular disease?
Regurgitation, dysphonia, dysphagia, laryngeal paralysis, weakness in intercostal and diaphragmatic muscles, contractures.
444
How can neuromuscular disease be distinguished from a spinal localisation (C1-T2)?
Neuromuscular disease may show pelvic and thoracic limb involvement, while a C6-T2 spinal cord lesion affects all four limbs or one side with decreased reflexes.
445
What are some differential diagnoses for myopathies?
Vascular ischaemic neuromyopathy, inflammatory/infectious myopathies, metabolic myopathies, breed-specific exercise-induced collapse, muscular dystrophies, neoplastic myopathies.
446
What are some differential diagnoses for junctionopathies?
Toxic botulism, tick paralysis, organophosphate/carbamate toxicity, snake bite, congenital and acquired myasthenia gravis, paraneoplastic syndrome.
447
What are some differential diagnoses for neuropathies?
Vascular ischaemic neuromyopathy, inflammatory/infectious polyneuropathies, toxic/drug-induced neuritis, metabolic neuropathies, idiopathic distal denervating disease, neoplastic neuropathies.
448
What investigations should be considered in neuromuscular cases?
Haematology and biochemistry, CK and electrolytes, imaging, infectious disease serology, neostigmine testing, electrodiagnostic tests, nerve and muscle biopsies.
449
What is Burmese hypokalaemia?
It is a genetic disease in Burmese cats causing muscle weakness and pain.
450
What imaging modality is excellent for evaluating cases with suspected inflammatory polyps?
CT
451
What type of enhancement is typically seen in inflammatory polyps?
Strong rim enhancement
452
What is the recommended imaging modality for identifying and classifying congenital malformations associated with vestibular disease?
MRI
453
Which nerves are most commonly affected in hypothyroidism?
Facial and vestibulocochlear nerves
454
What is the most common type of neoplasm associated with peripheral vestibular disease?
Ceruminous adenoma/adenocarcinoma
455
What imaging modality is usually recommended for evaluating extension and potential surgical evaluation of aural neoplasms?
CT or MRI
456
What tests are likely to be required for investigating central vestibular disease?
Blood tests, advanced imaging, cerebrospinal fluid collection
457
What type of vascular disease has been more recognized in dogs and cats since the availability of MRI?
Ischaemic and haemorrhagic cerebrovascular disease
458
What are some of the tests that should be undertaken to identify a possible underlying cause of vascular disease?
Specific blood tests, imaging of thorax and abdomen, urinalysis, and blood pressure
459
What is the dural-tail sign?
Thickening of the dura
460
Besides meningiomas, what other conditions can show the dural-tail sign?
Lymphoma, histiocytic sarcoma, and nerve sheath tumors
461
Which nutritional deficiency can cause involvement of the vestibular system?
Thiamine deficiency
462
What are the initial signs of thiamine deficiency?
Anorexia and lethargy
463
What can be a fatal outcome if left untreated?
Thiamine deficiency
464
What is the final effector of the motor unit?
Muscle
465
What are the essential components of each motor unit?
Motoneuron, neuromuscular junction, and muscle innervated
466
What is the functional cellular unit of skeletal muscle?
Myofibre
467
What components make up each muscle fibre?
Myofibrils and myofilaments (protein actin and myosin)
468
Which system is responsible for connecting the central nervous system with the muscle to be innervated?
Lower Motor Neuron system
469
What does the Lower Motor Neuron system include?
Cranial nerve nucleus or ventral horn cell body, axon, neuromuscular junction, and muscle innervated
470
What is neuromuscular disease?
A group of pathologies affecting the nerves, neuromuscular junction, and muscles with similar clinical signs
471
Which animals may develop thiamine deficiency due to a raw fish diet?
Cats
472
What is a possible outcome of early supplementation in thiamine deficiency?
Resolution of signs
473
Which animals may develop thiamine deficiency due to cooked meat or overheated food?
Dogs and cats
474
What are the presenting signs of meningoencephalitis of unknown origin?
Seizures, depression, circling, and visual deficits.
475
What is the basis of treatment for meningoencephalitis of unknown origin?
Immunosuppression.
476
Name some drugs used to treat meningoencephalitis of unknown origin.
Corticosteroids, cytarabine, cyclosporine, lomustine, mycophenilate, mofetil, leflunomide, and procarbazine.
477
What are the three groups of outcome/response to treatment for meningoencephalitis of unknown origin?
Poor prognosis, good response with long-term medication, and good response with eventual discontinuation of medication.
478
When is treatment generally recommended for meningoencephalitis of unknown origin?
When untreated, as these conditions are fatal.
479
What should be done if a patient is not clinically normal or experiences regular relapses when the dose is decreased?
Medication should be continued long-term with the lowest possible dose to control the disease.
480
What is the recommendation for medication discontinuation in normal patients of meningoencephalitis of unknown origin?
Ideally, an MRI should be repeated prior to discontinuation to check for any remaining lesions.
481
What is the role of the vestibular system?
The vestibular system is responsible for maintaining balance.
482
What are the common abnormalities associated with the vestibular system?
Changes in gait, head and body posture, and eye movement.
483
How can gait evaluation be useful for vestibular patients?
Gait evaluation helps with neuroanatomical localization and shows asymmetry.
484
What is the characteristic behavior of vestibular patients during gait?
They tend to fall, roll, and circle towards the side of the lesion.
485
What is a common clinical sign seen with vestibular patients?
Head tilt.
486
Does head tilt alone differentiate between peripheral and central pathology?
No, it does not differentiate and is usually towards the affected side.
487
How can hypertonia be elicited in vestibular patients?
By picking up the patient, turning into recumbency, and observing the limbs of the unaffected side.
488
What additional behavior suggests vestibular pathology?
Low stance, abnormal tail position, and jerky body movements towards the side of the lesion.
489
What is nystagmus?
Involuntary rhythmic oscillation of the eyes.
490
What is the purpose of nystagmus?
To stabilize the image on the retina and optimize image formation.
491
How can physiological nystagmus be elicited?
By moving the head side to side or up and down.
492
What does physiological nystagmus evaluate?
The vestibular system and sensory input.
493
What imaging modalities can be used to detect larger infarcts?
CT and MRI
494
What does a small infarct typically appear as on T1-weighted MRI?
Iso to hypointense
495
What imaging modality can provide information on the chronicity of an infarct?
Diffusion weighted imaging
496
What is a potential consequence of chronic ear disease?
Intracranial extension of otitis media / interna
497
How are radiographic changes of secondary meningoencephalitis in chronic ear disease often detected?
They can be extremely subtle
498
What imaging modalities are likely to show strong contrast enhancement and associated compression of the brainstem in meningoencephalitis?
Both CT and MRI
499
What is the preferred imaging modality for investigating caudal fossa pathology?
MRI
500
What type of tumours are difficult to differentiate from acoustic schwannomas on MRI?
Meningiomas and lymphoma
