vascular lesions of the CNS Flashcards
aneurysms
85% of subarachnoid haemorrhages are caused by aneurysms
Incidence of aneurysms = 1% of the population
Incidence of rupture causing SAH = 6-12 per 100,000 population per year
Some familial occurrence (probably associated with procollagen III deficiency)
Peak age 40-60 years, F:M 3:2 (varies with age)
Rarely seen in infants or children
aneurysms causes
Changes in the arterial walls:
Local thickening can occur at the intimal layer, proximal and distal to the branching site
This thickened area is not as elastic and can cause increased strain in the more elastic portions of the vessel wall
Abnormalities in structural proteins in the arterial walls have also been identified (Chyatte et al, 1990)
↑ risk with hypertension, smoking and alcohol, so they may be involved in the acquired vessel damage
Giant aneurysms are >2.5cm Occur at arterial bifurcations
sites of aneurysms
MCA 20-25%
ACOM 35-40%
PCOM 30%
PICA 10%
treatment
Surgical clipping
Endovascular coiling
Physiotherapy Implications:
Pre-treatment, patient is normally on bed rest, 15° head up
Post-treatment, await clearance from neurosurgeon (clipping) or interventional neuroradiologist (coiling) to mobilise
surgical clipping
Access through a craniotomy
Metal clip applied to the neck of the aneurysm
Aneurysm re-growth may occur if a portion of the neck lies
outside the clip
Clipping prevents re-bleeding
Small risk of clip migration, but rare
Prevents use of MRI in future diagnostic testing
SAH sub arachnoid haemorrhage
Accounts for 3% of all strokes (Sudlow & Warlow, 1997) but 5% of all stroke deaths
Incidence: 10-15 per 100,000 population
85% caused by rupture of an aneurysm
Clinical Features Severe unrelenting headache often described as a “thunderclap”, “worst headache imaginable” Vomiting (70%) Neck stiffness Seizure (6-16%) Reduced GCS Limb weakness Associated trauma
risk factors
non mod
mod
Sex: Females 1.6x
Race: African Americans 2.1x higher, higher incidence in Finland and Japan
Genetics: 5-20% of SAH sufferers have a positive family history
Autosomal dominant polycystic
kidney disease Smoking Hypertension Heavy Drinking Hormonal?
investigations
CT Scan: confirms SAH diagnosis in 95% of SAH if within 48 hours of the bleed
Lumbar Puncture : If CT negative or no focal signs on
assessment
MR Angiography: Detects aneurysms. A guide wire is inserted via the femoral vessels and contrast medium injected to allow detection of abnormalities. A mild anaesthetic is utilised and patient remains flat for approx 4 hours.
SAH complictions
High risk of cerebral ischaemia or infarction after SAH, especially 4-12
days after onset
Clinically patients can present as being cognitively “vague”
Vasospasm
Arterial narrowing evident on angiography Complex interaction of vasoconstrictive substances Risk of cerebral ischaemia
Managed with Triple H therapy: hypertension, hypervolemia, haemodilution
Hypovolemia and hyponatremia
“Cerebral salt wasting syndrome”: excessive renal secretions of Na2+ Fluid loss and reduced plasma volume
physiotherapy implications
On the one hand, mobilising too early could cause vasospasm and expand a neurological deficit; but on the other hand, the effects of immobility can also be detrimental.
Top Tips:
Liaise with team – outline the case for mobilising
Check vital signs before you start (especially HR and BP)
Close monitoring of patient’s cognitive abilities
Short but frequent bouts of activity at first
Bed-based exercises are better than no exercise
Care with drains: external ventricular drains (EVDs) are positioned at the level of the patient’s head and need to be clamped off before you move the patient!
physio after SAH rx
Similar approach to other stroke patients
Once mobilising, physio involvement depends on presence of
neurological (motor) deficits
RAMP Principles: aim for Restoration of movement
Prognosis depends on extent of initial deficit and cognitive involvement
Balance rehab
AVM
Developmental abnormalities of the intra- cranial vasculature
Firm tangled mass of blood vessels with small areas of haemorrhage, thrombosis and calcified nodules
Diminished blood-flow to surrounding areas
More likely to bleed in younger patients (20-
40y)
Risk of haemorrhage is 2-4% with a risk of re-bleeding increasing to 17%
clinical presentation of AVM
Haemorrhage (40-60%) Epilepsy Neurological deficit (large AVMs, close to basal ganglia) – “steal” effect Headache Incidental finding of cranial bruit
management
Surgical excision
Stereotactic radiosurgery
Embolisation by cerebral angiography
Occlusion of feeding vessels
physiotherapy
Indicated for patients with: neurological deficit
and / or reduced mobility post-intervention
Presentation often similar to a stroke (depending on site of AVM)
May have mobility restrictions in first 5-7 days post presentation
/ surgery – especially if vasospasm
Check with neurosurgical team
Once restrictions are lifted, proceed as normal, but be mindful
of neurological changes
