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Michaelmas 5th year > Neuro diseases of brain and cranial nerves > Flashcards

Neuro diseases of brain and cranial nerves Flashcards

1
Q

Some clinical signs of forebrain disease; mentation, cranial nerves, gait, postural reflexes, spinal reflex, sensation

A

Altered mentation; confused, depressed
Cranial nerves: reduced contralateral menace reflex
Gait = normal; may have head turn towards lesion, compulsive walking, head pressing
Postural reactions: decreased contralateral limb
Normal spinal reflexes
Reduced contralateral sensation

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2
Q

Two types of vascular infarct disease

A

Haemorrhagic vs ischaemic

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3
Q

What does fluid/fat look like on T2 MRI

A

Fluid is bright
Fat is bright

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4
Q

What does fluid look like on T1 weighted MRI

A

Fluid is dark (hypointense)

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5
Q

How does flair MRI work

A

T2 weighted but suppresses low protein fluids e.g CSF
BUT fluid in the cells looks bright e.g for avoiding masking of periventricular issues with bright ventricles full of CSF

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6
Q

What is normal vs abnormal CSF like

A

Normal = clear, low cells, low protein
Abnormal = abnormal colour e.g yellow suggests haemorrhage, thicker if infection present, increased cell number, increased protein, see neutrophils (not normally there)

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7
Q

What is empyema and what is a common cause

A

Build up of pus in the CNS; usually related to cat bites

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8
Q

What is meningo-encephaliits of unknow origin

A

Suspected autoimmune inflammation of brain and meninges
Including granulomatous and necrotising meningoencephalitis

More common in small breed females

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9
Q

Treatment of meningitis of unknown origin

A

Immunosuppressive doses of corticosteroids

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10
Q

Signs of congenital hydrocephalus

A

Large dome shaped head, altered mentation, difficulty training, circling, paresis, ventro-lateral strabismus, persistent fontanelle

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11
Q

Care with interpreting MRI showing enlarged ventricles

A

Does not necessarily mean it has hydrocephalus; if presenting later in life that is probably just their anatomy ad there is something else going on

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12
Q

Treatment of congenital hydrocephalus

A

Corticosteroids, omeprazole
(can use mannitol/hypertonic saline in an emergency to reduce intracranial pressure)

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13
Q

What is the surgical option for treating hydrocephalus

A

Ventriculo-peritoneal shunt placement; lots of complications

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14
Q

What is hepatic encephalopathy

A

When neurotoxic compounds like manganese, ammonia, glutamate reach the brain due to liver dysfunction
–> Could be liver disease, microvascular dysplasia, portosystemic shunts

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15
Q

How can we treat hepatic encephalopathy

A

Treat liver disease
Reduce circulating neurotoxins via a hypoallergenic diet/highly digestible proteins
+ lactulose can be used to select for bacteria that produce less ammonia and increases gut transit time

If there is a porto-systemic shunt, can ligate once the patient is stable

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16
Q

Whcih animals do we tend to see hypoglycaemia in

A

Young, toy or hunting breeds

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17
Q

What is the diagnosis of hypoglycaemia

A

Serum blood glucose <3.3mmol/l along with clinical signs e.g serizures, lethargy, tremors, altered mentation, icnreased appetite, signs worsening with exercise

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18
Q

What are some possible underlying causes of hypoglycaemia

A

Insulinoma, liver disease, sepsis, xylitol toxicity, atypical Addison’s, insulin overdose, glycogen storage diseases, starvation, parasitism, GIT disease

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19
Q

What must we be careful about when supplementing glucose in hypoglycaemia cases esp with insulinomas

A

Rebound hypoglycaemia

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20
Q

What are intra-axial tumours

A

ONes that arise from brain parenchyma e.g glioma, ependymoma, pituitary tumours, choroid plexus tumours

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21
Q

What are extra-axial tumours

A

Arise from extra-parenchymal tissue e.g meninges or bones
esp meningioma

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22
Q

What type of brain tumours are brachycephalics mostly affected by

A

Gliomas

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23
Q

What type of brain tumours are dolichocephalic breeds affected by mostly

A

Meningiomas

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24
Q

What treatment approach would we take with gliomas

A

Radiotherapy due to deep, hard to access position in the brain

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25
Q

What is the prognosis like for meningiomas

A

Very good in cats

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26
Q

What is canine cognitive dysfunction

A

Degenerative condition in older animals showing progressive senile behaviours

MRI may show brain atrophy, enlargement of ventricles, wide culci

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27
Q

What is in the peripheral and central parts of the vestibular system

A

Peripheral: sensory receptors in inner ear, vestibulocochlear nerve

CEntral: vestibular nuclei in brainstem, inhibitory influence from cerebelum, [influence from thalamus, cranial cervical spin]

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28
Q

Signs of vestibular disease

A

Head tilt towards side of disfunction due to reduction in extensor tone
Nystagmus
Vestibular ataxia; esp when blindfolded
Wide base stance (poor balance)

29
Q

Which direction does fast and slow phase of nystagmus go

A

Fast phase runs away from lesion

30
Q

What type of lesions is vertical nystagmus assocaited with

A

Central vestibular lesions

31
Q

Main differences on exam between central and peripheral vestibular disease

A

Postural reactions are normal in peripheral disease but MAY be abnormal on side of lesion in central disease

Horner’s syndrome is strongly assocaited with peripheral disease

If paresis is present suggests central

32
Q

What is paradoxical vestibular disease

A

A head tilt on the opposite side to a cerebellar lesion due to loss of usual inhibitory input from cerebellum to the vestibular system
So get relatively less input on contralateral side and head tilt towards this

33
Q

What degenerative disease might affect the vestibular system

A

Lysosomal storage disease

34
Q

What nutritional disease might affect the vestibular system and what type of disease

A

Thiamine deficiency
= central vestibular disease

35
Q

What toxic cause might give vestibular disease

A

Metronidazole

36
Q

What type of vestibular disease would a cerebrovascular incident give

A

Central

37
Q

What signs do we get with cerebrovascualr accident

A

Central vestibular signs with peracute onset
Minimal progression and gradual improvement

38
Q

What would we see on MRI with a cerebrovascular accident ischaemic lesion

A

Hyperintense, sharply marginated lesion of mainly grey matter confined to vascular territory of affected vessel

39
Q

What would we see on MRI with a cerebrovascular accident haemorrhagic lesion

A

Mass lesion with intensity varying over time

40
Q

What concurrent diseases can lead to ischemic and haemorrhagic cerebrovascular accidents

A
  • Ischaemic: endocrine disorders (anything causing hypercoagulable state), renal, cardiac, neoplasia, sepsis, parasitic, hypertension
  • Haemorrhagic: neoplasia, coagulopathy, parasitic (e.g angiostrongylus), malformations, trauma, hypertension, vasculitis
41
Q

Which is more common out of ischaemic vs haemorrhagic causes of cerebrovascular accident and which has better prognosis

A

Ischemic accounts for 70%; and has better prognosis

42
Q

What type of vestibular disease does FIP cause and how

A

Central
Related to immune-complex mediated vasculitis

43
Q

What other sign is CNS form of FIP often assocaited with

A

Uveitis; ocular form
non-effusive

44
Q

Treatment of FIP

A

Remdesivir
Adenosine nucleoside analogue GS-441524

45
Q

What vestibular signs can metronidazole therapy cause

A

CEntral, subacute/acute onset, progressive signs

E.g cerebellovestibular ataxia, head tilt, nystagmus, seizures (Since affects forebrain too)

46
Q

How can we speed up the recovery from metronidazole therapy after stopping drug

A

Diazepam

47
Q

What kind of vestibular disease can hypothyroidism lead to

A

Both central disease (via CVA ischaemic from atherosclerosis via altered lipid metabolism)
and peripheral disease (polyneuropathY)

48
Q

What might a cat with central vestibular bilateral disease, walking close to ground, tail up and head swaying have

A

Thiamine deficiency

49
Q

How does thiamine deficiency cause central vestibular signs

A

Via encephalopathy due to impairment of energy metabolism causing lactic acidosis and gluatamate release

Predeliction for medial vestibular nuclei

50
Q

What is the most common cause of vestibular disease in cats (second most common in dogs)

A

Otitis media/interna

51
Q

Why can’t we excluse inflammatory otitis from being a cause of vestibular disease after a clear otoscope examination

A

Because only 30% of cats with otitis media interna have otitis externa

52
Q

What other deficits might we see with otitis media

A

Facial nerve deficits
Sympathetic supply to the eye deficits

53
Q

What signs do we get with inflammatory polyps causing vestibular issues

A

Peripheral vestibular disease with subacute/acute onset and progressive
Mostly young, male cats

Often concurrent horner’s disease (since localised in middle ear)

54
Q

What drugs can cause toxic vestibular disease peripherally

A

Aminoglycosides
Tetracyclines
CHlorhexidine in perforated tympanus

55
Q

What is the most common cause of vestibular disease in dogs

A

Idiopathic
= diagnosis fo exclusion
Give supportive treatment and most resolve in a few weeks

= peripheral disases

56
Q

What does the vestibulocerebellum do

A

Gives inhibitory input onto the vestibular system

57
Q

Signs of cerebellar dysfunction

A

Hypermetria
Truncal sway
Tremor
Vestibular signs = paradoxical vestibular disease on contralateral side to the lesion
Absent ipsilateral menace
Abnormal ipsilateral proprioception

58
Q

What inflammatory infection can cause cerebellar disease and how do we treat

A

Neospora (has a cerebellar predilection)
Treat with clindamycin

59
Q

MRI signs with neospora causing cerebellar disease

A

Atrophied cerebellum means lots of CSF fluid and space around the cerebellum

60
Q

What is little white shaker disease

A

Steroid responsive tremor syndrome
= a fine tremor that disappears with rest typicaly in young animsl

61
Q

How do we treat steroid responsive tremor syndrome and what do we need to consider before this

A

Use immunosuppressive steroid doses
Be sure that it isn’t neospora causing cerebellar signs before starting this

62
Q

What is cerebellar abiotrophy

A

Where dogs are born normal but there is later degeneration of cerebellar cells
No treatment
Progressive

63
Q

Signs of Horner’s syndrome

A

Miosis, ptosis, enophthalmus
+ protrusion of third eyelid, red conjunctiva due to vessel vasodilation

64
Q

Signs of idiopathic facial neuropathy

A

Abnormal facial expression
Loss of palpebral and corneal reflexes
Dropping of food or saliva from mouth
Reduced tear production/dry nose due to parasympathetic part of faical nerve being damaged too

May have idiopathic vestibular syndrome

65
Q

Treatment of idiopathic facial neuropathy

A

None
- eye lubrication important

66
Q

What is idiopathic trigeminal neuropathy

A

A suspected autoimmune neuritis most commonly affecting the mandibular branch of the trigeminal nerve

67
Q

Signs of idiopathic trigeminal neuropathy

A

Dropped jaw (if bilateral), difficulty prehending food, masticatory muscle atrophy, may see horners

68
Q

Treatment and prognosis for idiopathic trigeminal neuropathy

A

No treatment
Most eat unassisted in weeks and recover fully

69
Q
A

Michaelmas 5th year (41 decks)

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