Common brain diseases Flashcards
(79 cards)
1
Q
A
2
Q
Mentation of forebrain diseases
A
Altered
Depression
Confusion
Abnormal
Behaviour
Delirium
3
Q
Cranial nerve reflexes in forebrain disease
A
Contralateral blindess
Decreased/absent menace with normal PLR
4
Q
Posture/gait in forebrain diseases
A
Usually normal
May have body or head turn
Compulsive wandering
Head pressing
Wide circles
5
Q
Postural reactions in forebrain disease
A
Decreased in contralateral limbs
6
Q
Spinal reflexes in forebrain diseases
A
Unaltered to increase in contralateral limbs
7
Q
Sensation in forebrain diseases
A
Reduced sensation contralateral face/body
8
Q
Other signs of forebrain diseases
A
Seizures
Neck pain
Movement disorders
Hemineglect syndrome
(narcolepsy, cataplexy)
9
Q
Mentation in brainstem lesions
A
Depressed
Stupor
Coma
10
Q
Cranial nerve deficits in brainstem disease
A
CN III-XII
11
Q
Posture/gait in brainstem disease
A
Ipsilateral hemiparesis/plegia
Tetraparesis/plegia
Vestibular ataxia (drifting, falling to side of lesion)
Head tilt
Decerebrate rigidity
12
Q
Postural reactions in brainstem diseases
A
Decreased ipsilateral limbs, thoracic and pelvic, or all 4 limbs
13
Q
Spinal reflexes in brainstem diseases
A
Normal to increased in all four limbs, or ipsilateral thoracic and pelvic limbs
14
Q
Sensation in brainstem disease
A
Unaltered
15
Q
Other signs of brainstem disease
A
Neck pain
Cardiac and respiratory abnormalities
16
Q
Mentation in cerebellar disease
A
Unaltered
17
Q
Cranial nerve deficits in cerebellar disease
A
Ipsilateral menace deficit with NORMAL vision and facial motor function
ANisocoria
Vestibular signs (paradoxical)
18
Q
Posture/gait of cerebellar disease
A
Intention tremor
Dysmetria
Hypermetria
Broad-based stance
Truncal sway
Decerebellate rigidity
19
Q
Postrual reactions in cerebellar diseases
A
Delayed initiation then exaggerated placement (dysmetria)
20
Q
Spinal reflexes in cerebellar disease
A
Normal
21
Q
Sensation in cerebellar disease
A
Normal
22
Q
Other signs of cerebellar disease
A
Increased frequency of urination
23
Q
Vascular brain diseases
A
Infarct; haemorrhagic vs iscaemic
24
Q
Bacterial brain diseases
A
Empyema (more in cats)
Abscess
Meningitis
25
Viral brain diseases
Canine disteper virus
Feline infectious peritonitis (FIP)
26
Fungal brain diseases
Cryptococcus
Aspergillus
27
Protozoal brain diseases
Toxoplasma
Neospora
28
Other infectious causes of brain disease
Rickettsial
Algal
29
Sterile inflammatory brain diseases
MUO
30
Anomalous causes of brain disease
Congenital hydrocephalus
Chiari malformation
Other
- lissencephaly
- meningomyelcele
- hydrancephaly
- porencephaly
- intracranial cysts
31
Toxic causes of brain disease
Metronidazole
Pyrethrin
Ivermectin
Xylitol
Etc...
32
Metabolic causes of brain disease
Hepatic encelopathy
Electrolyte imbalances
Hypoglycaemia
Uremic encelopathy
33
Idiopathic causes of brain disease
Narcolepsy
Epilepsy
Movement disorders
34
Neoplastic brain diseases
Intra-axial
Extra-axial
Metastatic
35
Nutritional causes of brain disease
Thiamine deficiency
Cobalamin deficiency
36
Degenerative causes of brain disease
Canine cognitive dysfunction (CCD)
'In born error of metabolism'
- Lysosomal storage diseases
- mitochondrial encelopathy
- organic acid urea
37
Lab and ancillary tests for brain disease
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
38
Advanced imaging for brain diseases
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
39
Cerebrospinal fluid (CSF) analysis
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
40
Risks of CSF tap
Haemorrhage
Infection
Damage to underlying neuronal structures
41
Contraindications of CSF tap
Herniation
Skin infection
Coagulopathy
42
Flair MRI of brain
To see periventricular tissue
43
T2 contrast in brain MRI
Fluid and fat bright
44
T1 + contrast brain MRI
Contrast shows increased blood flow/ neovascularised tumours)
45
Brain infarct
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
46
What underlying conditions can predispose a brain infarct
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)
47
Clinical signs of brain infarct
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
48
Treatment of brain infarct
Manage clinical signs and supportive care
Manage any underlying disease
Outcome usually good where no underlying disease
49
Meningoencephalitis (MUO/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
50
Three main subtypes of MUO
Granulomatous meningoencephalitis (GME)
Necrotising meningoencephalitis (NME)
Necrotising leukoencephalitis (NLE)
A lot of overlap and often cannot be distinguished
51
Diagnosis of MUO
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
52
Treatment of MUO
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
53
Negative prognostic indicators for MUO
Seizures
herniation
inflammation in CSF at 3 month recheck
If survive over 3 months tend to survive long term
54
Canine cognitive dysfunction (CCD)
Chronic, progressive, 'senile' behaviours
Older dogs <9 and cats >12
55
Diagnosis of Canine cognitive dysfunction (CCD)
Owner questionnaires and perception of behaviour
Rule out other potential causes
MRI - brain atrophy
56
Treatment of canine cognitive dysfunction (CCD)
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
57
Canine distemper virus
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
58
Clinical signs of canine distemper virus
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
59
Treatment for canine distemper virus
No specific treatment
Supportive care:
- fluid therapy
- pain relief
- anti-epileptic dugs
Prognosis usually poor
Disease is often fatal
60
Feline infectious peritonitis (FIP)
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
61
Most common neuroogical signs of FIP
Seizures
Cerebellar signs
Vestibular dysfunction (bilateral)
Tetraparesis
Systemic signs in many but not all cats:
anorexia
weight loss
pyrexia
ocular signs
62
Diagnosis of FIP
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
63
Treatment of FIP
Disease progresses over severeal weeks
100% fatal
No definitive treatment
Corticosteroids used as palliative treatment to reduce associated inflammation
64
Congenital hydrocephalus
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
65
Clinical signs of congenital hydrocephalus
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
66
Diagnosis of congenital hydrocephalus
Challenging as enlarged ventricular system does not define hydrocephalus
Must be seen with concurrent clinical signs
Ultrasound through an open fontanelle
CT or MRI
67
Treatment of congenital hydrocephalus
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
68
Hepatic encelopathy
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
69
Clinical signs of hepatic encephalopathy
Mentation changes
Seizures
Ptyalism
Signs of liver dysfunction
- vomiting
- weight loss
- anorexia
- jaundice
70
Diagnosis of hepatic encephalopathy
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
71
Treatment of hepatic encephalopathy
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
72
Hypoglycaemia (neurological signs)
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
73
Clinical signs of hypoglycaemia
Seizures
Lethargy/weakness
Tremors
Increased appetite
Altered mentation
Central blindness
74
Diagnosis of hypoglycaemia
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
75
Treatment of hypoglycaemia
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
76
Brain neoplasia
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
77
Signalment of brain neoplasia
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
78
Clinical signs of brain neoplasia
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
79
Treatment of brain neoplasia
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
