Brain disease Flashcards
(30 cards)
Where can the brain herniate in ICP?
forebrain herniates underneath the tentorium cerebelli or cerebellum herniates through the foramen magnum
What are the signs of raised ICP?
• POOR mental status - ARAS • Cushing’s reflex • pupil size and PLR • vestibular eye movement - MLF • abnormal postures decerebrate decerebellate
Outline the cushings reflex
• bradycardia & hypertension
• ICP increases above MAP resulting in cerebral ischaemia
• α-1-adrenergic sympathetic activation → systemic
vasoconstriction → hypertension
• carotid artery baroreceptors detect hypertension → vagal activation → bradycardia
Outline pupil size as ICP increases
anisocoria to
bilateral pinpoint to
bilateral dilated not responsive to light.
N.B loss of physiological nystagmus = early sign of raised ICP
Why does decerebellate positioning often occur?
Often d/t herniation of the cerebellum
Can be positional
What are the main brain diseases based on VITAMIN D?
V – CVA - ischaemic or hemorrhagic strokes
I – MUOs, “White shakers”, bacterial ME, protozoal MEs (Toxoplasma, Neospora), viral MEs (CDV, FIP, FIV), fungal MEs
T – head trauma, many toxins
A – hydrocephalus, lissencephaly, hydranencephaly and porencephaly, CCA
M – hepatic encephalopathy, hypoglycaemia, electrolyte imbalances
I
N – meningiomas, gliomas, pituitary tumours, lymphoma, metastases, MPNST
D – lysosomal storage diseases, cognitive dysfunction, many degenerative GM and WM disorders
What is white shakers?
• mostly young small breed dogs of any colour • fine tremor – rapid, low amplitude, worse with stress/excitement, +/- other deficits: • head tilt, reduced menace response, ataxia, opsiclonus • Diagnosis: • CSF – very mildly inflammatory • +/- MRI to rule out other problems • Treatment: • corticosteroids for 4-6m • +/- other immunosuppressive drugs • diazepam initially • fair to good px, can relapse immune mediated dz
Outline bacterial meningitis
- 3 main routes of infection:
- haematogenous
- direct invasion (ear, eyes, nose, bone, bite wounds)
- CSF
- usually acute CNS signs (obtundation and CN deficits most common)
- neck pain (~30%)
- pyrexia and neutrophilia in about 50%
- CSF
- increased protein concentration and pleocytosis
- phagocytosed organisms in CSF rare
- CSF/blood culture (positive ~15-30%) – inside abscess or in small amounts
- antibiotics +/- surgical drainage
- guarded prognosis
What are the types of injury in head trauma?
Primary - • physical disruption of parenchyma • concussion • contusion • laceration • no intervention possible
Secondary - release of inflammatory mediators
continued haemorrhage
leads to ↑ ICP (oedema, haemorrhage)
the aim of our intervention
How can you use the modified Glasgow coma scale?
useful for serial monitoring
↑ score → better prognosis
What are the aims of IVFT?
restore intravascular volume to ensure adequate CPP
hypotension significantly increases mortality
resuscitation then maintenance
avoid glucose containing fluids as hyperglycaemia is associated with a poorer outcome
Outline the use of mannitol with raised ICP
↓ blood viscosity, ↑ CBF and oxygen delivery, free radical scavenger, osmotic effect
0.5-1g/kg slow bolus over 20m
follow with crystalloid therapy to prevent dehydration
contraindicated in hypovolemia
Outline the use of 7.5% saline in raised ICP
• hyperosmotic agent, free radical scavenger • 4 ml/kg of 7.5% as slow bolus • contraindicated: • hyponatraemia • cardiac or respiratory disease reverses shock • decreases ICP • increases CBF and oxygen delivery
What are some considerations with pain in raised ICP
pain increases blood pressure and therefore ICP
caution as morphine may cause emesis and result in increased ICP
Outline general care in head trauma patients
keep head elevated (~30°)
avoid jugular compression
turn q4-6h
Cathterise and get feeding tube in some way
Outline hydrocephalus
• abnormal dilation of ventricular system within cranium
• toy breeds, young age
• domed shaped head, persistent fontanelle, abnormal
behaviour, cognitive dysfunction, obtundation, circling,
pacing, seizures (?), vestibular signs
• treatment:
• medical (corticosteroids, furosemide, AEDs)
• surgical (VP shunt)
What is lissencephaly?
cerebrum has smooth surface without development of gyri and sulci
seizures, behaviour changes
Lhasa Apso, Korat cat
What is hydrancephaly/ porencephaly
presence of cerebral cavities, usually communicating with subarachnoid space and/or lateral ventricles
signs in 1st few months (circling, abnormal behaviour) or up to few years (seizures)
Outline brain neoplasia
more common in older and larger breed dogs • most common clinical signs • seizures in supratentorial tumours • central vestibular dysfunction in infratentorial tumours • median survival time 69 days • infratentorial tumours 28 days • supratentorial tumours 178 days • treatment • less sedative AEDs • anti-inflammatory doses of prednisolone • analgaesia (paracetamol, gabapentin) • surgery +/- RT
Outline hepatic encephalopathy
- reversible neurological manifestations secondary to any aetiology of acute or chronic liver failure (generally PSS)
- pathogenesis is multifactorial, complex and poorly understood
- hyperammonemia + neuroinflammation + cerebral oedema + deranged neurotransmission
- vague signs - failure to thrive, weight loss, PU/PD, GI signs
- forebrain signs: behaviour changes, blindness, seizures, etc
- rare brainstem or cerebellar signs reported in older dogs
- diagnosis relies on bile acid stimulation test, fasting ammonia, ultrasound or CT angiography
How do you treat hepatic encephalopathy
lactulose
• traps ammonia as non-diffusible ammonium in intestinal lumen, decreases absorption of ammonia through cathartic effect and inhibits uptake of glutamine by intestinal wall
antibiotics
• reduce ammonia-producing bacteria in the gut
• diet
• aim to reduce gut derived blood ammonia
• restricted protein content, aromatic amino acids and short chain fatty acids
minimising contributing factors that:
• increase ammonia production (constipation, GI bleeding, azotemia, infection, hypokalemia)
• reduce clearance of toxins (dehydration, hypotension, anaemia)
• affect neurotransmission (benzodiazepines)
• seizure control (levetiracetam, KBr, PB, propofol)
How does low BG affect the brain?
- glucose is major carbohydrate substrate of brain
- glucose oxidation is primary source of energy
- brain consumes ~25% of total blood glucose
- brain has 3x metabolic rate of peripheral tissues but 10-30% less extracellular glucose
- lack of glycogen stores in the CNS
- insulinomas, juvenile hypoglycaemia, hepatic dysfunction
- Clinical signs:
- anxiety, lethargy, depression
- ravenous appetite, exercise intolerance
- tremors, visual deficits, seizures, coma
Outline low sodium causing brain signs
major extracellular ion in the body
• blood levels reflect ratio of sodium to water in extracellular fluid and account for most of the osmotically active particles in serum
• signs of forebrain dysfunction (altered mentation, blindness, seizures, coma)
• slow correction is essential
• oral administration safer when possible
• acute onset - 1mEq/l per hour
• chronic onset - 0.5 mEq/l per hour
What are the degenerative brain diseases
• storage diseases - defect of a lysosomal enzyme
• accumulation and storage of substrate(s) within the
cytoplasm of neurons, as well as in cells in other
organs
• early onset
• diffuse neurological dysfunction
• progressive course, leading to death
• abiotrophies, axonopathies, leukodystrophies, etc…
• other late-onset degenerative disorders such as
Lafora disease
