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VetMed Year 4- Term 1 > NEUROLOGY WEEK 1 > Flashcards

NEUROLOGY WEEK 1 Flashcards

1
Q

A head tilt is often due to

A

Vestibular disease

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2
Q

A head turn is often due to

A

Forebrain disease (turned towards sign of lesion)

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3
Q

Decerebrate body posture is ___.

Is indicitive of a lesion where?

A

Extention of all limbs and opistontonosis (exten of head/neck). Associated with stuperous./ comatose state.

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4
Q

Decerebellate body posture is ____.

Is indicitive of a lesion where?

A

DecereBELLATE is opthistonosus with thoracic limbs extended but hips flexed. Mentation normal. Indicitive of Cerebellar lesion

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5
Q

Schiff-Sherrington posture is ___.

Indicitive of a lesion where?

A

Acute severe thoracic/ cranial lumber spinal cord lesion. \
Extensor of thoracic limbs
Paralysis of Pelvic limbs (reflex preserved)

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6
Q

UMN Paresis gait

A

Muscle tone and Spinal reflexes - Normal to increased tone caudal to lesion

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7
Q

LMN Paresis gait

A

Muscle tone decreased. Bunny hopping / Knuckling.

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8
Q

The spinal cord is split into what 4 sections for localisation of lesions

A

C1-C5
C6-T2
T3-L3
L4-Cd

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9
Q

Which nerve does the Biceps tendon reflex test

A

Musculocutaneous (C6-C8)

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10
Q

Which nerve does the Triceps tendon reflex test

A

Radial n (C7-T2)

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11
Q

Which nerve does the Patellar tendon reflex test

A

Femoral n (L4-L6)

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12
Q

Which nerve does the Gastroc tendon reflex test

A

Sciatic n (L6-S2)

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13
Q

The pelvic limb withdrawal reflex tests which nerve and spinal cord segment

A

Sciatic nerve. L6-S2. (same as Gastroc tendon reflex)

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14
Q

Pathway for the Menace response

A

Is a CORTICAL response.

II–>Forebrain–>Cerebellum–> Brainstem–> VII

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15
Q

Pathway for the PLR reflex

A

Is a SUBCORTICAL response.

II–>Brainstem–>III

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16
Q

Pathway for Palpebral reflex

A

Facial sensation.

V –> Brainstem –> VII

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17
Q

Inability to close the jaw would be indicitive of a lesion in which CN

A

Trigeminal control motor to muscles of mastication.

Atrophy/ Inability to close the jaw.

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18
Q

Difference between a Simple focal and Complex focal seizure

A

Simple focal: no loss of consciousness

Complex focal: impairement of consciousness

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19
Q

Status Epilepticus is a seizure for > ___min

A

Seizure lasting more than 5 minutes (clinical)

More than 30 minutes = brain damage

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20
Q

Define cluster seizure

A

> 2 seizures in 24 hour period = serious.

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21
Q

Define Prodrome, Aura, Ictus and Post-ictal

A

Prodrome: Behaviour changes that happen days/hours before seizure
Aura: Sensory/Focal onset on seizure (difficult to see in animals)
Ictus: Seizure event
Post-Ictal: Neurological alterations post seizure

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22
Q

5 finger neurology rule

A
  1. Onset
  2. Clinical curse
  3. Pain
  4. Lateralising
  5. Neurological localisation
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23
Q

Which DAMINNT cause Lateralisation?

A

Degenerative, Neoplastic, Inflamm/Infectous, Trauma/ Vascular

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24
Q

What does DAMNITV stand for

A

Degenerative, Anomaly, Metabolic, Neoplastic/Nutritional/ Inflamm/Infectious/Idiopathic/Trauma/Toxic/ Vascular

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25
Q

Which DAMNITV cause pain?

A

Degenerative, Neoplasia, Infect, Inflamm, Trauma , Vascular

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26
Q

Which DAMNITV cause acute onset

A

Trauma, Toxic, Vascular

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27
Q

Waxing and Waning onset is especially indicitive of which type type of neuropathology

A

DAMNITV. Metabolic causes waxing and waning onset. Also not painful and not lateralising.

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28
Q

Acute onset but improving rather than deteriorating is indicitive of what…

A

DAMNITV. Trauma/Vascular tend to improve over type post acute onset. Also painful.

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29
Q

If Menace response is abnormal but palpebral reflex normal, what does this tell you about CN VII

A

Menace: CN II -> Forebrain –> Cerebellum–> Brainstem –> CN VII
Palpebreal: CN V–> Brainstem –> CN VII
Tells you facial nerve is normal.

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30
Q

Which crystals in urine are highly suggestive of a portosystemic shunt

A

AGE= METABOLIC = WAXING AND WANING
Ammonium biurate crystals (sharp crystals_ = highly suggestive
Also biochem = low liver enzymes/ creatinine/cholesterol. Related to feeding?

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31
Q

Diagnostic tests for portosystemic shunt

A

Ultrasound liver/ biochem/ Fasting bile acids

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32
Q

In human epilepsy patients, over expression of ___ is thought to change local brain uptake

A

Over expression of p-glycoprotein (PGP)

= PharmacoRESISTANT epilepsy in humans

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33
Q

When to start epilepsy treatment

A

More than 1 seizure every 6 weeks. Or more isolated within 6 weeks.
Status epilepticus or cluster seizures (within 24 hr period)
CHRONIC DISEASE

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34
Q

Treatment of Status epilepticus

A

Status: Seizure >30 mins in duration (or >5 mins clinicalls)

Benzodiapines or Phenobarbitone

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35
Q

How do Barbiturates/ Benzodiapines work for treatment of status epilepticus?

A

Barbiturate: Increase durating of Cl- channel opening. increased EFFICIENCY
Benzodiaz: Increased frequency of Cl- = Increased POTENCY

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36
Q

What effects would you expect to see on biochemistry on phenobarbital epilepsy treatment?

A

ALP elevation is common.
Side effects: Sedation, PD, Polyphag, Hepatotoxicity (metabolised by liver).
ROUTINE BIOCHEM BILE ACID STIM q 6 mnts

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37
Q

What tests should be done every 6-12 months on phenobarbital treatment

A

MONITOR phenobarb levels.
Routine biochem (raised ALP is common)
Bile acid stim test

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38
Q

Which rare but severe idiosyncratic reactions can occur with phenobarbital treatment.
What action should be taken?

A

Behavioural alterations.
Immune mediated neutropenia, thrombocytopenia, anaemia secondary to bone marrow necrosis.
Superficial necrolytic dermatitis.
STOP DRUG IMMEDIATELY

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39
Q

How does the time to steady state vary between Phenobarbital and Potassium Bromide

A

Phenobarbital: 10-14 days (half life 24 hrs)

Potassium Bromide: 100-200 days (half life 14 days)

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40
Q

When should plasma levels of a) KBr and b) Phenobarbital be taken

A

a) KBr: 4 weeks

b) Phenobar: 14 days

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41
Q

How does excretion route vary between phenobarb and KBr

A

Phenobarb: Liver metabolised (hence common increase in aLP/ Hepatotoxicity)
KBr: Renal excretion

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42
Q

Seizures are normally the result of involvement of the __-

A

Forebrain involvement

can be caused by extracraninal causes e.g. metabolic

43
Q

What diet can influence serum concentration of Potassium Bromide?

A

High chloride in the diet can lower serum concentration of Potassium Bromide

44
Q

What toxicity is associated with KBr?

How is it treated?

A

RARE.
Severe ataxia, sedation, skin reaction.
Normally due to renal insufficiency (as renally excreted c.f. phenobarb = liver)
THERAPY = IV FLUIDS TO INCREASE EXCRETION

45
Q

Which seizure therapy does not require serum drug monitoring?

A

Imepitoin,
Not recommended for status epilepticus or cluster seizures in cats.
Only licenced for idiopathic epilepsy in dogs

46
Q

Therapeutic index for Imepitoin

A

No ideosyncreatic reactions have been observed.
Drugs appears safe with good therapeutic index..
NO EFFECT ON LIVER ENZYMES

47
Q

When is Imepitoin indicated

A

First line treatment for dogs with newly diagnosed idiopathic epilepsy (no serum monitoring required).
NOT for cluster seizures/ status epilepticus or in cats
Good for patients that have side effects on phenobarb.

48
Q

Patients can develop tolerance to which antiepilpetic drug

A

Phenobarb/

49
Q

A ‘non-responder’ to anti-epilepsy medication is a patient whose seizure frequency doesn’t reduce below ___ %

A

Below 50% reduction in seizure frequency = failure.

50
Q

2 add on drugs for refractory seizures and there side effects

A
  1. Gabapentin - sedation ataxia

2. Levetiracetam - Sedation (rare)

51
Q

First and second choice AED’s for cats

A
  1. Phenobarb (polyphag, bone marrow suppression, cutaneous hypersensitivity)
  2. Diazepam (hepatotoxicity- contraindic in liver disease)
    Diazepam can’t be used in dogs as develop tolerance.
52
Q

Why is KBr not used in cats with epilepsy

A

Bronchial asthma

53
Q

Status epilepticus up to 30 minutes leads to

A

Stress response: Arterial hypertension, Increased cerebral blood flow, Hypoxemia, Hypercarbaemia, HYPERglycemia, lactic acidosis

54
Q

Status epilepticus >30 minutes leads to

A

Continous muscle contraction. Hyperthermia, Acidosis, Myolysis- hyperkalemia- renal failure.
HYPOglycemia
Hypotension
Cardiac arrthymias

55
Q

Post status epilepticus considerations

A

minimise brian injury., Treat hypotension - supplement O2.. Treat hypotension, volume expansion.
Monitor electrolytes.
Minimise hyperthermia./ renal impairment
TREAT UNDERLYING DISEASE
- Hypoglycemia? Toxicity?? - DIURESIS

56
Q

Ataxia is divided into what 3 types

A
  1. Sensory
  2. Vestibular
  3. Cerebellar
57
Q

Clinical signs of Sensory ataxia

A

Abnormal postural reactions. Limb paresis - knuckling.

Wide based stance/ increased stride length.

58
Q

Clinical signs of Vestibular ataxia

A

Heat tilt, learning, falling or rolling to one side. Abnormal nystagmus. NORMALLY TILT TOWARDS SIDE OF LESION

59
Q

Clinical signs of Cerebellar ataxia

A

Cerebellum fine tunes movement

- Wide based stance, intention tremors of the head. Loss of balance/truncal sway

60
Q

A wide based stance is indicative of ___ ataxia

A 
Cerebellar ataxia. 
Wide based stance
Intention trmors of the head.
Loss of balance and truncal sway. 
Ipsilateral meance defects with normal vision (II-->Forebrain-->Cerebellum--> Brainstem--> VII
61
Q

Which breed of cat has a congenital nystgamus>

A

Siamese

62
Q

Ptosis is

A

‘drooping’ or falling of the eyelid. Clinical sign of Horners syndrome alone with Enophtalmos (posterior displacement of globe into orbit)

63
Q

Additional clinical sign of Horner’s syndrome in horse

A
  • Ptsosis (drooping of eyelid)
  • miosis
  • Enophtalmus (posterior displacement of globe)
  • Prominant third eyelid
  • Conjunctival/Nasal hyperaemia
  • SWEATING!! See regional sweating pattern, follows symph
64
Q

Function of the Saccule and Urticule

A

Head position/gravity.

Semicircular canals = head motion/ angular acceleration.

65
Q

Cerebellum is primarily ______ to vestibular nuceli

A

Cerebellum is primarily INHIBITORY to vestibular nuclei.
Signs of cerebellar ataxia: Wide base stance, intention tremors of the head, ipsilateral menace deficits with normal vision

66
Q

A rotary jerk nystagmus can’t be seen in what species?

A

Can’t be seen in dogs as pupil is round.

67
Q

How can CENTRAL vestibular and PERIPHERAL vestibular disease be differentiated

A

Rotary/Horizontal nystagmus can be either central/peripheral.
Vertical Nystagmus can only be central vestbular.

68
Q

Horners syndrome is more likely to be CENTRAL/PERIPHERAL vestibular?

A

More likely to be peripheral vestibular.

Rare for horners syndrome to be caused by central.

69
Q

Vertical nystagmus is CENTRAL/PERIPHERAL VESTIBULAR DISEASE?

A

Vertical nystagmus = Central vestibular.

70
Q

Which cranial nerves affected in a) central b) peripheral vestibular disease

A

a) central. CN V-XII

b) Peipheral: CN VII only

71
Q

Peripheral vestibular disease STEP 1 is to determine if…

A

Ototoxic drugs have been given. If given, STOP.
If not given- otoscopic examination. Check if otitis media, interna or neoplasia.
Myringtotomy

72
Q

Rostral lobe cerebellar ataxia

A

Decerebellate posture (optistontonus, forelimb hyperextention, hindlimb flexion))

73
Q

Hypermetria and Intention tremor is indicitive of ____ataxia

A

Caudal lobe Cerebellar ataxia

74
Q

What would you expect if the Flocculonodular lobe was affected by cerebellar ataxia

A

Dysequilibrium. Broad based gait

75
Q

Paradoxical vestibular signs are expected when which part of cerebellum is damaged

A

Caudal cerebellar peduncle = cerebellar ataxia.
With paradoxical vestibular = HEAD TILT IS OPPOSITE to SITE of lesion,
With central vestibular= HEAD TILT IS SAME SIDE AS LESION

76
Q

The reticular activating system is a network of nerves with pathways to the ___

A

forebrain

77
Q

Ddx of Mentation changes causes by neurological disorder

A

Changes in mentation can be due to neurological disorders but can also be due to systemic disorder e.g. pyrexia/ hypertension

78
Q

Forebrain is divided into what 3 areas

A
  1. Association area- Cerebral cortex- Neocortex
  2. Emotion area- Limbic systemic - Archicortex
  3. Olfactory area- Olfactory bulb (Paleocortex)
79
Q

The limbic system is

A

The second part of the forebr5ain - emotion area- archicortex

80
Q

Pleurothotonus is

A

head turn/ turning of the body

81
Q

Forebrain syndrome includes

A
  1. Altered mentation
  2. Pacing/ Head pressing/ Pleurothotonus
  3. Decreased/ absent menace response with normal PLR (see pathway)
  4. Deficits to contralateral limb
  5. Normal/increasd reflexes in contralateral limb
    Muscle tone can be increased.
82
Q

Cranial nerves exiting the brainstem include

A

III-XII. Also contains vestibular system

83
Q

Brainstem syndrome

A

Paresis- all 4 limbs, or ipsilateral), opisthotonus, Decerebrate posture (posit, extension all4 limbs)
Spinal reflexes normal to increased in all OR IPSILATERAL limbs (c.f. forebrain syndrome)
Decreased sensation (face)

84
Q

Pacing/ head pressing is indicative of

A

Forebrain syndrome.
Altered meance response/ normal PLR.
Increased/normal spinal reflxes and muscle tone in contralateral limb.
c.f. brainstem syndrome= ipsilateral

85
Q

From what age is the menace reponse present

A

Cortical response.

From 12 weeks old.

86
Q

A medial strabismus would be indicative of damage to which nerve/

A

Abducens = innervates Lateral rectus therefore damage to this would lead to medial strabismus

87
Q

Sensory innervation to the a) medial canthus of eye b) lateral canthus of eye

A

a) medial = ophthalmic branch
b) lateral = maxillary branch
Of trigem

88
Q

Sensory ‘taste’ to Rostral 2/3rds of tongue is suppled by

A

taste to the rostral 2/3rd of the tongue is fungiform papillae which are innervated by facial nerve (chorda tympani branch),

89
Q

Sensoneural deafness is linked to

A

White coat and blue eyes. e.g. merle gene.
Dalmation.
Hiar cells die at 3-4 weeks.
Most common cause of Sensoineureal deafness is Otitis Interna

90
Q

3 causes of Conductive deafness

A

Neoplasia, Infection (otitis media) inflamm (polyp in cats)

91
Q

Larangeal sensation and Larynx / Pharynx motor supplied by

A

Vagus X

92
Q

Inspiratory dysnoea, most likely cause

A

Vagus brances to recurrent larangeal nerve.

93
Q

4 causes of Acquired Megaoesophagus

A

CARE ASPIRATION PNEUMONA

  1. Hypoadrenocorticoism (addisions)
  2. Myasehtesia Gravis
  3. Oesophagitis
  4. Botulism
  5. BRAINSTEM DISEASE
94
Q

What would be the effect on a) vision b) menace c) PLR of a lesion at the optic chiasm

A

NO VISION, NO MENACE AND NO PLR BILATERALLY

95
Q

Treatment for Permetherin toxicity

A

Decontaminate bath - WARM, TOOHOT may increase absorption.
Activated charcoal.
Duazepam/ Propofol infusion.

96
Q

Cerebral hypoplasia in a calve most likely due to

A

BVDV - Pestivirus (RNA)

Same as border disease in lambs ‘hairy shaker lamb’

97
Q

Cerebellar hypoplasia in a kitten with voming, dirrhoea and reduced white blood cells most likely

A

Feline panleukopenia virus (cat equiv of parvo BUT parvo has no cerebellar hypoplasia)

98
Q

2 diseases that cause cerebellar hypoplasia in calves

A

Smallenberg, blue tongue, BVDV

99
Q

Horse spinal cord with haemorrhage/ infarct/ necrosis ‘spheroids’ - likely virus?

A

EHV-1 respiratory and neurological.

100
Q

EHV-1 pathogenesis of neurological signs

A

Only effects spinal cord. Attacks endothelium causes arteritis. Thrombus causes necrosis - infarction of axons- respond by swelling forming ‘ spheroids’

101
Q

Diagnosis of EHV-1

A

CSF tap.

ISOLATE HORSES. Don’t move on to or off yard

102
Q

Type of virus that causes FIP.

How does it causes CNS signs?

A

Cornavirus Dry form causes granulomatous lesions.

Wet form = effusion’

103
Q

Piglet with nystagum, paddling movement of the limbs. Necrospy reveals widespread haemorrgage and prulent exudate / meningitis. Likely pathogen =

A

Strep suis.

Extensors stronger than flexors. Less inhibition from UMN.

VetMed Year 4- Term 1 (12 decks)

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