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SA Neurology > Common brain diseases > Flashcards

Common brain diseases Flashcards

1
Q

Mentation of forebrain diseases

A

Altered
Depression
Confusion
Abnormal
Behaviour
Delirium

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2
Q

Cranial nerve reflexes in forebrain disease

A

Contralateral blindess
Decreased/absent menace with normal PLR

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3
Q

Posture/gait in forebrain diseases

A

Usually normal
May have body or head turn
Compulsive wandering
Head pressing
Wide circles

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4
Q

Postural reactions in forebrain disease

A

Decreased in contralateral limbs

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5
Q

Spinal reflexes in forebrain diseases

A

Unaltered to increase in contralateral limbs

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6
Q

Sensation in forebrain diseases

A

Reduced sensation contralateral face/body

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7
Q

Other signs of forebrain diseases

A

Seizures
Neck pain
Movement disorders
Hemineglect syndrome
(narcolepsy, cataplexy)

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8
Q

Mentation in brainstem lesions

A

Depressed
Stupor
Coma

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9
Q

Cranial nerve deficits in brainstem disease

A

CN III-XII

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10
Q

Posture/gait in brainstem disease

A

Ipsilateral hemiparesis/plegia
Tetraparesis/plegia
Vestibular ataxia (drifting, falling to side of lesion)
Head tilt
Decerebrate rigidity

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11
Q

Postural reactions in brainstem diseases

A

Decreased ipsilateral limbs, thoracic and pelvic, or all 4 limbs

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12
Q

Spinal reflexes in brainstem diseases

A

Normal to increased in all four limbs, or ipsilateral thoracic and pelvic limbs

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13
Q

Sensation in brainstem disease

A

Unaltered

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14
Q

Other signs of brainstem disease

A

Neck pain
Cardiac and respiratory abnormalities

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15
Q

Mentation in cerebellar disease

A

Unaltered

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16
Q

Cranial nerve deficits in cerebellar disease

A

Ipsilateral menace deficit with NORMAL vision and facial motor function
ANisocoria
Vestibular signs (paradoxical)

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17
Q

Posture/gait of cerebellar disease

A

Intention tremor
Dysmetria
Hypermetria
Broad-based stance
Truncal sway
Decerebellate rigidity

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18
Q

Postrual reactions in cerebellar diseases

A

Delayed initiation then exaggerated placement (dysmetria)

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19
Q

Spinal reflexes in cerebellar disease

A

Normal

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20
Q

Sensation in cerebellar disease

A

Normal

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21
Q

Other signs of cerebellar disease

A

Increased frequency of urination

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22
Q

Vascular brain diseases

A

Infarct; haemorrhagic vs iscaemic

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23
Q

Bacterial brain diseases

A

Empyema (more in cats)
Abscess
Meningitis

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24
Q

Viral brain diseases

A

Canine disteper virus
Feline infectious peritonitis (FIP)

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25
Q

Fungal brain diseases

A

Cryptococcus
Aspergillus

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26
Q

Protozoal brain diseases

A

Toxoplasma
Neospora

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27
Q

Other infectious causes of brain disease

A

Rickettsial
Algal

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28
Q

Sterile inflammatory brain diseases

A

MUO

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29
Q

Anamolous causes of brain disease

A

Congenital hydrocephalus
Chiari malformation
Other
- lissencephaly
- meningomyelcele
- hydrancephaly
- porencephaly
- intracranial cysts

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30
Q

Toxic causes of brain disease

A

Metronidazole
Pyrethrin
Ivermectin
Xylitol
Etc…

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31
Q

Metabolic causes of brain disease

A

Hepatic encelopathy
Electrolyte imbalances
Hypoglycaemia
Uremic encelopathy

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32
Q

Idiopathic causes of brain disease

A

Narcolepsy
Epilepsy
Movement disorders

33
Q

Neoplastic brain diseases

A

Intra-axial
Extra-axial
Metastatic

34
Q

Nutritional causes of brain disease

A

Thiamine deficiency
Cobalamin deficiency

35
Q

Degenerative causes of brain disease

A

Canine cognitive dysfunction (CCD)
‘In born error of metabolism’
- Lysosomal storage diseases
- mitochondrial encelopathy
- organic acid urea

36
Q

Lab and ancillary tests for brain disease

A

Haematology
Biochemistry (electrolytes, liver function, glucose)

Young dog, with suspected impaired liver funtion: bile acid stimulation test

Vascular causes suspected: blood pressure and coagulation tests

Thyroid disease suspected: T4/TSH

Urinalysis with culture

Older dogs: thoracic radiographs for mets

37
Q

Advanced imaging for brain diseases

A

MRI - most detail of the intracranial soft tissues

CT - useful for the assessment of more crude lesions and lesions within a bony compartent. Much quicker so good for traumatic brain injury.

Can use a contrast medium

38
Q

Cerebrospinal fluid (CSF) analysis

A

Taken from cisterna magna following advanced imaging

Should be clear and colourless with few/no cells and low protein

Abnormalities:
- pleocytosis (increased no of cells)
- increased protein
- abnormal colour (yellow= previous haemorrhage)
- Rarely cells from exfoliative tumours can be seen

Can be tested for infectious agents using PCR or serology

Must be performed under GA

39
Q

Risks of CSF tap

A

Haemorrhage
Infection
Damage to underlying neuronal structures

40
Q

Contraindications of CSF tap

A

Herniation
Skin infection
Coagulopathy

41
Q

Flair MRI of brain

A

To see periventricular tissue

42
Q

T2 contrast in brain MRI

A

Fluid and fat bright

43
Q

T1 + contrast brain MRI

A

Contrast shows increased blood flow/ neovascularised tumours)

44
Q

Brain infarct

A

Tissue damage caused by the sudden interruption of blood supply to an area or organ.

Ischaemic (more common) or haemorrhagic

Sight hounds and CKCS predisposed

45
Q

What underlying conditions can predispose a brain infarct

A

Make a patient hypercoagulable or affect vessel wall integrity - found in 50% of dogs presenting with brain infarction

Hyperadrenocorticism

Renal disease

Hypertension

Cardiac disease

Protein losing enteropathy/nephropathy

Disseminated intravascular coagulation

Many other hormonal, inflammatory, neoplastic diseases

Septic focus - endocarditis/abscess (septic emboli)

46
Q

Clinical signs of brain infarct

A

Per-acute
Non-progressive
Static after 24hours
Usually focal and asymmetric

Signs representative of where the lesion lies

Rostral cerebellar arterial is predilection sight for dogs: cerebellar or vestibular signs

47
Q

Treatment of brain infarct

A

Manage clinical signs and supportive care

Manage any underlying disease

Outcome usually good where no underlying disease

48
Q

Meningoencephalitis (MUO/A)

A

Inflammation of the brain and meninges

Thought to be an autoimmune process

Sterile - no infectious cause found

More common in small breed female dogs, but can be any dog or cat

49
Q

Three main subtypes of MUO

A

Granulomatous meningoencephalitis (GME)

Necrotising meningoencephalitis (NME)

Necrotising leukoencephalitis (NLE)

A lot of overlap and often cannot be distinguished

50
Q

Diagnosis of MUO

A

Exclusion of other causes

Routine haematology and biochemistry to exclude metabolic

MRI - should reveal the multifocal changes throughout the parenchyma

CSF analysis - marked inflammatory cells

51
Q

Treatment of MUO

A

Suppression of immune system

Long courses of immunosuppressive of corticoid steroids e.g. prednisolone

Dose tapered over a few months

Often second immunosuppressive agent added: cytarabine, ciclosporine, or lomustine

52
Q

Negative prognostic indicators for MUO

A

Seizures
herniation
inflammation in CSF at 3 month recheck

If survive over 3 months tend to survive long term

53
Q

Canine cognitive dysfunction (CCD)

A

Chronic, progressive, ‘senile’ behaviours

Older dogs <9 and cats >12

54
Q

Diagnosis of Canine cognitive dysfunction (CCD)

A

Owner questionnaires and perception of behaviour

Rule out other potential causes

MRI - brain atrophy

55
Q

Treatment of canine cognitive dysfunction (CCD)

A

Medications
- selegiline (monoamine oxidase B inhibitor)
- vivitonin
- gabapentin/pregablin (GABA-ergic)
- TCAs/SSRAs/trazadone (anxiolytics)

Diets
- antioxidant, essential FAs, met
- Hills B/d
- purine NC neurocare
- Purine one viprant maturity 7+

Supplements and environmental enrichment

56
Q

Canine distemper virus

A

Disease in the acute phase by replicating in neurons and glial cells - degenerative lesions within the central nervous sytem

Chronic phase - late immune response to CDV develops, inflammatory demyelinating lesions

Usually seen in puppies or juvenile dogs

57
Q

Clinical signs of canine distemper virus

A

The result of a multifocal central nervous system disorder and include seizures, visual deficits, cerebellar signs, vestibular dysfunction, paresis, and myoclonus.

Myoclonus characteristic.

Systemic signs: respiratory and GI involvement

Ocular lesions: chorioretinits

58
Q

Treatment for canine distemper virus

A

No specific treatment

Supportive care:
- fluid therapy
- pain relief
- anti-epileptic dugs

Prognosis usually poor
Disease is often fatal

59
Q

Feline infectious peritonitis (FIP)

A

Feline coronavirus

Very common in cats but usually causes GI disease, FIP occurs when inappropriate immune response to virus

Neurological form more common in non-effusive, dry form.

Induces a pyogranulomatous and immune complex-mediated vasculitis

Common cause of meningoencephalitis

60
Q

Most common neuroogical signs of FIP

A

Seizures
Cerebellar signs
Vestibular dysfunction (bilateral)
Tetraparesis

Systemic signs in many but not all cats:
anorexia
weight loss
pyrexia
ocular signs

61
Q

Diagnosis of FIP

A

None definitive

MRI:
- ventricular dilation (pbstructive hydrocephalus)
- lack of suppression of CSF on FLAIR sequences
- inflammation of the meninges
- ependyma
- choroid plexus

Complete cell count abnormalities
- anaemia +/- leukocytosis

Biochemistry
- normal or:
- hypoalbuminaemia
- hyperglobulinaemia
- albumin/globulin

Feline coronavirus antibody titres

CSF
- neutrophilic pleocytosis
- marked increase in protein concentration

62
Q

Treatment of FIP

A

Disease progresses over severeal weeks

100% fatal

No definitive treatment

Corticosteroids used as palliative treatment to reduce associated inflammation

63
Q

Congenital hydrocephalus

A

Predominantly small toy breeds (chihuahua, brachycephalic)

Usually <1year, commonly under 6months

Usually no underlying cause, thought to be dysfunction in CSF production, absorption, and flow

Rarely due to a stenosis of the mesencephalic aqueduct causing a physical obstruction

64
Q

Clinical signs of congenital hydrocephalus

A

Large or domed shaped skull with or without:
- persistent fontanelle
- ventral and lateral strabismus
- altered mentation
- difficulty/loss of training
- circling
- paresis
- blindness
- seizures
- vestibular dysfunction

65
Q

Diagnosis of congenital hydrocephalus

A

Challenging as enlarged ventricular system does not define hydrocephalus

Must be seen with concurrent clinical signs

Ultrasound through an open fontanelle

CT or MRI

66
Q

Treatment of congenital hydrocephalus

A

Can be medical or surgical

Medical:
- reducing production of CSF and enhancing the absorption with administration of oral corticosteroids
- omeprazole (may reduce CSF production)
- mannitol and/or hypertonic saline reduces intracranial pressure

Surgical:
- ventriculoperitoneal shunt

67
Q

Hepatic encelopathy

A

Occurs when liver function is compromised

Occurs due to organ failure, microvascular dysplasia or portosystemic shunting

Signs of encephalopathy occur due to neurotoxic compounds reaching the brain without being detoxified by the liver

Specific toxins include: manganese, ammonia, glutamate

68
Q

Clinical signs of hepatic encephalopathy

A

Mentation changes
Seizures
Ptyalism

Signs of liver dysfunction
- vomiting
- weight loss
- anorexia
- jaundice

69
Q

Diagnosis of hepatic encephalopathy

A

Documenting hepatic dysfunction with bile acid stimulation test, ammonia levels, liver markers on biochemistry

Haematology: microcytic anaemia

Liver enzymes normal or elevated

U/S used to confirm presence of portosystemic shunt (PSS)

CT angiogram

70
Q

Treatment of hepatic encephalopathy

A

Treat underlying liver disease

Treat any associated seizures and reduce the circulating neurotoxins

Dietary modulation by feeding high quality and highly digestible protein

Lactulose: increased time in gut, selects for bacteria that produce less ammonia, creates an ammonia trap by creating an acidic environment

Control seizures e.g. levetiracetam and potassium bromide (not metabolised in liver)

Surgical ligation of a PSS

Prognosis extremely variable

71
Q

Hypoglycaemia (neurological signs)

A

Neurological signs as glucose needed for energy in CNS

Causes variable:
- insulinoma
- liver disease
- sepsis
- xylitol toxicity
- atypical Addison’s
- glycogen storage diseases
- iatrogenic (insulin overdose)

Young, toy, or hunting breeds are predisposed following a period of anorexia, extreme exertion, or gastroenteritis/parasitic infection

72
Q

Clinical signs of hypoglycaemia

A

Seizures
Lethargy/weakness
Tremors
Increased appetite
Altered mentation
Central blindness

73
Q

Diagnosis of hypoglycaemia

A

Serum blood glucose below 3.3mmol/l with consistent clinical signs

Routine haematology and biochemistry to look for underlying causes, and abdominal U/S

CT for insulinoma and microadenomas

74
Q

Treatment of hypoglycaemia

A

Depends on underlying cause

Oral supplementation of glucose either with feeding or in acute episodes honey or glucogel on gums

IV glucose bolus can result in rebound hypoglycaemia

75
Q

Brain neoplasia

A

Intra-axial: arising from brain parenchyma
- gliomas
- choroid plexus tumours
- ependymomas
- pituitary tumours

Extra-axial: from extraparenchymal origin such as meninges or bone
- meningiomas

Metastatic:
- haemangiosarcomas
- lymphomas
- mammary gland tumours
- other carcinomas

76
Q

Signalment of brain neoplasia

A

Older animals

> 95% dogs diagnosed are >5years

Median age at diagnosis 9 years in dogs and 11 years in cats

Golden retrivers, labradors, collies, dobermans, boxers, can be any breed

Dolicephalic breeds: meningiomas
Brachycephalic breeds: gliomas

Cats: meningioma and lymphoma

77
Q

Clinical signs of brain neoplasia

A

Relate to location of tumour or secondary effects of tumour (raised intracranial pressure)

Most commonly in forebrain so seizures

Other clinical signs: circling, altered mentation, head turn

Can have a normal neurological exam

If pituitary tumour can have endocrine signs

78
Q

Treatment of brain neoplasia

A

Meningioma: often superficial and only locally invasive so good for removal

Gliomas: deep in parenchyma so surgical removal challenging, radiotherapy more suitable

Radiation therapy: reduction of tumour size, can have reasonable outcomes

Chemotherapy: controls tumour growth, rarely used unless lymphoma, need to pass BBB e.g. lomustine - gliomas, cytosine arabinoside - lymphoma, hydroyurea - meningiomas.

Anticonvulsie drugs for secondary effects of tumour

SA Neurology (11 decks)

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