Lyrics · 完整歌詞
In acute ischaemic stroke,
the duration and severity of impaired perfusion help determine
which tissue is irreversibly injured and which may still be salvaged.
Ischaemia exhausts ATP, the sodium-potassium pump fails,
water enters the cell and cytotoxic oedema precedes death.
About 1.9 million neurons die in each untreated minute,
and each hour ages the brain by 3.6 years.
A sudden focal deficit is stroke until proven otherwise.
The first test is non-contrast CT to exclude haemorrhage,
because a normal early CT never excludes infarction.
Ischaemic subtypes carry their own signatures.
Large artery atherosclerosis produces cortical signs such as aphasia, neglect and hemianopia.
Cardioembolism from atrial fibrillation is maximal at onset
and may strike several territories.
Lacunar infarcts from hyaline perforators give pure motor or pure sensory syndromes
and never cortical signs.
The thalamus gives contralateral pure sensory loss,
the ventral pons a locked-in state with only vertical gaze,
and the lateral medulla the Wallenberg syndrome.
There a single posterior inferior cerebellar artery silences crowded neighbours at once:
crossed pain and temperature loss, Horner syndrome, dysphagia and hoarseness,
vertigo and ipsilateral ataxia.
In acute ischaemic stroke,
the duration and severity of impaired perfusion help determine
which tissue is irreversibly injured and which may still be salvaged.
Around the dead core lies the penumbra,
tissue perfused at roughly 25 to 50 per cent that is electrically silent
yet structurally alive.
Alteplase within 4.5 hours rescues it.
Beyond that window the failing blood-brain barrier turns reperfusion into symptomatic haemorrhage
in about six per cent,
outweighing what remains to save.
Thrombectomy for large vessel occlusion extends to 6 to 24 hours
when perfusion imaging shows a small core and a large penumbra,
as DAWN and DEFUSE-3 demonstrated.
Before thrombolysis the blood pressure must fall below 185 over 110.
Without thrombolysis,
pressures up to 220 over 120 are tolerated
so that the penumbra is not starved.
Cardioembolic stroke is prevented thereafter with anticoagulation, the rest with antiplatelet therapy,
statins and blood pressure control.
Haemorrhage names its cause by location.
Deep bleeding in the putamen, thalamus,
pons or cerebellum comes from hypertensive Charcot-Bouchard microaneurysms;
lobar bleeding in the elderly comes from amyloid angiopathy.
Systolic pressure is lowered towards 140 mmHg,
corticosteroids are withheld because they harm without helping,
and a cerebellar haematoma over three centimetres is evacuated.
Thunderclap headache with neck stiffness is subarachnoid haemorrhage until proven otherwise.
When CT is negative, lumbar puncture seeks xanthochromia,
and nimodipine 60 mg four-hourly for 21 days guards against vasospasm,
which peaks between days 4 and 14.
Moyamoya narrows the terminal carotid and the anterior and middle cerebral origins
while sparing the posterior circulation;
children present with ischaemia, adults with haemorrhage,
and bypass surgery is the treatment.
Survival is only the first half.
Broca aphasia is non-fluent with preserved comprehension, Wernicke fluent but uncomprehending,
conduction aphasia fails at repetition, and the transcortical aphasias preserve it.
The Barthel index scores ten basic activities and excludes medication and finances.
Shoulder-hand syndrome spares the elbow, a subluxed shoulder must never be pulled,
and spasticity responds to baclofen and botulinum toxin.
Venous thrombosis is prevented by early mobilisation rather than bed rest.
In acute ischaemic stroke,
the duration and severity of impaired perfusion help determine
which tissue is irreversibly injured and which may still be salvaged.