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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2612_Библиотеки_им_академика_М_И_Перельмана
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Opening the floodgates
(a)
(b)
https://t.me/med1917
In
1935
, the Hoover Dam (fig
umph of engineering, began to nourish and power a parched Southwest
10.14
) on the Colorado River, an unprecedented tri-
USA
. 6.6
million tonnes of steadfast concrete served the altogether unanticipated function
of symbolizing perseverance amid the depths of the Great Depression. We are unequipped to understand disconnect between structure and function in the human
body. The dualistic mind– brain rift deepened in the
disorders fell beyond the grasp of the organically rooted doctor. A naturalistic
20
th century and functional
philosophy of medicine would even
discount these as diseases entirely.
What then do we say to the person
who shudders without seizing, or
who senses without feeling? Their
account wouldn’t satisfy any perception of ‘health’. ‘Draining the symptoms dry’ is a good place to start.
Asking them to list all their symptoms saves rather than costs time.
Demonstrate paradoxical findings
to the patient, such as Hoover’s sign
(functional weakness of hip extension
returns to normal during contralateral hip flexion against resistance).
The understanding that structure
may not be determining function can
be therapeutic in itself.
461
3
10 Neurology
Fig 10.
14
(a) The Hoover Dam, Bureau of Reclamation, public domain work of US government.
23
(b) Hoover sign in a
asks him to raise his left leg as she holds her hand under his right heel. B, Revealing his lack of
eort, the patient exerts so little downward force with his right leg that she easily raises it.
C, When she asks him to raise his right leg while cupping his left heel, the patient reveals his
intact strength as he unconsciously forces his left ‘paretic’ leg downward. D, As if to carry the
example to the extreme, the patient forces his left leg downward with enough force to allow
her to use his left leg as a lever to raise his lower torso.
-year-old man who has a psychogenic left hemiparesis. A, Neurologist
(b) Reproduced from Kaufman et al., Kaufman’s Clinical Neurology for Psychiatrists
Source: (a) US Bureau of Reclamation. https:// www.usbr.gov/ lc/ hoover dam/ ;
(2022), with permission from Elsevier under the STM Agreement.
10 Neurology
Acute bilateral leg weakness
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462
It is crucial to establish a diagnosis quickly to avoid permanent disability. Look for specific patterns (see later in topic) and ask these questions to help elicit the diagnosis:
1
Where is the lesion? • Are the legs flaccid or spastic? (ie
sensory loss? A sensory level usually means spinal cord disease.
LMN
or
of bowel or bladder control? (Lesion more likely to be in the conus medullaris or
cauda equina.)
2
What is the lesion? • Was ons et sud den or rap idl y p rogr essi ve? This is a n em er-
gency; it suggests cord compression or spinal stroke so get urgent help (see next
paragraph).
CRP
Cord compression (See also p
weakness— often less severe— suggests a cervical cord lesion, see
level ± preceding back pain (
• Are there any signs of infection (eg tender spine, T°,
: extradural abscess)?
524
.) Symptoms Bilateral leg weakness (arm
p
538
). Bladder (and anal) sphincter involvement is late
and manifests as hesitancy, frequency, and, later, as painless retention.
for a motor, reflex, and sensory level, with normal findings above the level of the
LMN
lesion,
the level (but remember tone and reflexes are usually reduced in acute cord compression;
kidney) in the spine is commonest. Rarer: infection (epidural abscess), cervical disc
prolapse, haematoma (warfarin), intrinsic cord tumour, atlanto- axial subluxation,
myeloma.
syphilis), spinal artery thrombosis or aneurysm, trauma, Guillain– Barré syndrome
(
liable;
to identify the nature of any mass. Do a
aries,
Tre at me nt Give urge nt de xamet hasone in mali gnan cy ( p
signs at the level (especially in cervical lesions), and
OHCS
p
562
). Causes Secondary malignancy (breast, lung, prostate, thyroid,
Transverse myelitis, MS, carcinomatous meningitis, cord vasculitis (
p
500
). Investigations Do not delay imaging at any cost. Spinal X- rays are unre-
MRI
is the definitive modality. Biopsy or surgical exploration may be needed
TB
). Bloods:
FBC, ESR, B
, syphilis serology,
12
CXR
(primary lung malignancy, lung second-
U&E, LFT, PSA
, serum electrophoresis.
524
) while considering more
specific therapy, eg radiotherapy or chemotherapy ± decompressive laminectomy;
which is most appropriate depends on tumour type, quality of life, and likely prognosis. Epidural abscesses must be surgically decompressed and antibiotics given.
Cauda equina and conus medullaris lesions The big dierence between these
lesions and those high up in the cord is that leg weakness is flaccid and areflexic, not
spastic and hyperreflexic.
lumbosacral nerve lesions.
Causes As above, plus congenital lumbar disc disease and
Signs Conus medullaris lesions feature mixed
signs, leg weakness, early urinary retention and constipation, back pain, sacral sensory disturbance, and erectile dysfunction. Cauda equina lesions feature back pain
and radicular pain down the legs; asymmetrical, atrophic, areflexic paralysis of the
legs; sensory loss in a root distribution; and sphincter tone; do
PR
Other patterns of leg weakness
DM
Unilateral foot drop
Weak legs with no sensory loss
, common peroneal nerve palsy, stroke, prolapsed disc, MS.
MND
, polio, parasagittal meningioma (an excep-
tion to the rule that weak legs mean cord or distal lesion).
Chronic spastic paraparesis
syringomyelia, subacute combined degeneration of the cord (
spastic paraparesis, taboparesis (tertiary syphilis, see
MS,
cord primary malignancy/ metastasis,
p
408
), histiocytosis X,
parasites (eg schistosomiasis).
Chronic flaccid paraparesis Peripheral neuropathy, myopathy.
Absent knee jerks and extensor plantars (Ie combined
cervical and lumbar disc disease, conus medullaris lesions,
LMN
or
UMN
MND
Fri edr eic h’s atax ia, su bac ute co mbi ne d d ege nera tio n o f t he co rd, tab op ares is.
UMN
?) • Is there
• Is there loss
WCC
,
ESR
p
504
) a sensory
Signs Look
UMN
signs below
PAN
UMN/ LMN
.
p
330
MND
), hereditary
signs.) Combined
, myeloradiculitis,
4
,
,
,
4
Tertiary syphilis (p
duced tone and tendon reflexes (without weakness). Later, additional involvement of the pyramidal tracts
causes taboparesis— a spastic paraparesis with the peculiar combination of extensor plantars (from the
taboparesis) and absent tendon reflexes (from the tabes dorsalis).
408
): in tabes dorsalis the aerent pathways from muscle spindles are lost, with re-
Gait disorders
https://t.me/med1917
Spastic Sti, circumduction of legs ± scung of the toe of the shoes:
UMN
lesions.
Extrapyramidal Flexed posture, shuing feet, slow to start, postural instability,
eg Parkinson’s disease.
Apraxic Pathognomonic ‘gluing- to- the- floor’ on attempting walking or a wide-
based unsteady gait with a tendency to fall, like a novice on an ice- rink. Seen in
normal pressure hydrocephalus and multi- infarct states.
Ataxic Wi de- based; falls; cannot walk heel- to- toe. Caused by cerebellar lesions (eg
MS
, posterior fossa tumours, alcohol, phenytoin toxicity); proprioceptive sensory
loss (eg sensory neuropathy,
B
). Often worse in the dark or with eyes closed.
12
Myopathic Waddling gait, cannot climb steps or stand from sitting due to hip
girdle weakness.
Fun ctio nal Suspect if there is a bizarre gait not conforming to any pattern of or-
p
ganic gait disturbance and without any signs when examined on the couch (
Tests Spinal X- rays;
electrophoresis;
MRI; FBC; ESR
CXR; LP; EMG
; syphilis serology; serum
; muscle ± sural nerve biopsy.
B
;
U&E; LFT; PSA
12
460
; serum
Non- neurological considerations in paralysed patients
Avoid pressure sores by turning and review weight- bearing areas often. Use
appropriate pressure- relieving mattresses/ cushions. Prevent thrombosis in
paralysed limbs by frequent passive movement, pressure stockings, and
p
346
). Bladder care is vital; catheterization is only one option (do not control
(
LMWH
incontinence by decreasing fluid intake). Bowel evacuation may be manual or
aided by suppositories; increasing dietary fibre intake may help. Exercise of unaected or partially paralysed limbs is important to avoid unnecessary loss of
function.
463
).
10 Neurology
10 Neurology
Abnormal involuntary movements (dyskinesia)
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464
These are characterized by impairment of the planning, control, or execution of
movement. They can have multiple manifestations:
Tremor Note frequency, amplitude, and exacerbating factors (stress; fatigue).
• Rest tremor Abolished on voluntary movement. Cause: parkinsonism (p
• Intention tremor Irregular, large- amplitude, worse at the end of purposeful acts, eg
finger- pointing or using a remote control. Cause: cerebellar damage (eg
• Pos tural t remor Absent at rest, present on maintained posture (arms outstretched)
and may persist (but is not worse) on movement. Causes: essential tremor (autosomal dominant; improves with alcohol), thyrotoxicosis, anxiety, - agonists.
Re- emergent tremor Postural tremor developing after a delay of ~10s. Causes:
Parkinson’s disease (don’t mistake for essential tremor).
Chorea Non- rhythmic, jerky, purposeless movements flowing from one place to
another— eg facial grimacing, raising the shoulders, flexing/ extending the fingers.
Causes Sydenham’s chorea (rare complication of group A streptococcal infection).
Huntington’s disease Incurable, progressive, autosomal dominant, neurodegenera-
tive disorder presenting in middle age, often with prodromal phase of mild symptoms (irritability, depression, incoordination). Progresses to chorea, dementia ± fits
15
(within ~
to expansion of
but trials for antisense oligonucleotides are underway. Counselling for patient and
family. Worsened by levodopa.
Hemiballismus Large- amplitude, flinging hemichorea (aects proximal muscles)
contralateral to a vascular lesion of the subthalamic nucleus (often elderly diabetics). Recovers spontaneously over months.
Athetosis Slow, sinuous, confluent, purposeless movements (especially digits,
hands, face, tongue), often dicult to distinguish from chorea.
is cerebral palsy (
classed as dystonias.
Tics Brief, repeated, stereotyped movements which patients may suppress for a
while. Tics are common in children (and usually resolve). In Tourette’s syndrome
(
clonidine if tics are severe (haloperidol may help but risks tardive dyskinesia).
Myoclonus Sudden involuntary focal or general jerks arising from cord, brainstem,
or cerebral cortex, seen in metabolic problems, neurodegenerative disease (eg
lysosomal storage enzyme defects),
spasms, juvenile myoclonic epilepsy).
with frequent generalized myoclonus, without progression. Often autosomal dominant. It may respond to valproate, clonazepam, or piracetam.
flap’)
from loss of extensor tone— ie incoordination between flexors and extensors
(= ‘negative myoclonus’).
thalamic stroke (consider if unilateral).
Tardive syndromes Delayed onset yet potentially irreversible symptoms occurring
after chronic exposure to dopamine antagonists (eg antipsychotics, antiemetics).
Classification •Tardive dyskinesia: orobuccolingual, truncal, or choreiform move-
ments, eg vacuous chewing and grimacing movements.
tained, stereotyped muscle spasms of a twisting or turning character, eg retrocollis
and back arching/ opisthotonic posturing.
or unease ± repetitive, purposeless movements (stereotypies, eg pacing).
myoclonus.
esia
help. Quetiapine, olanzapine, and clozapine are examples of atypical antipsychotics
that are less likely to cause tardive syndromes.
yrs of diagnosis). Atrophy and neuronal loss of striatum and cortex, due
CAG
repeat on Chr. 4. (p70). No treatment prevents progression,
OHCS
p
262
). Most other ‘athetoid’ patterns may now be better
Pseudoathetosis Caused by severe proprioceptive loss.
p
690
), motor and vocal tics occur. Consider psychological support, clonazepam or
CJD
(p
483
), and myoclonic epilepsies (infantile
Benign essential myoclonus Childhood onset
Jerking (~1– 2 jerks/ s) of outstretched hands, worse with wrists extended,
Causes Liver or kidney failure, Na+ , CO2, gabapentin,
• Tardive akathisia: sense of restlessness
• Tardive tourettism (p
Gradually withdraw neuroleptics and wait 3– 6 months. Tetrabenazine may
690
). • Tardive tremor. Treating tardive dyskin-
Causes Commonest
Asterixis (‘metabolic
• Tardive dystonia: sus-
490
MS
, stroke).
• Tardive
).
Dystonia
https://t.me/med1917
Dystonia describes prolonged muscle contractions causing abnormal posture or
repetitive movements.
Idiopathic generalized dystonia Childhood- onset dystonia often starting in one
leg with ipsilateral progression over
DYT1
common (
(needs an
brain stimulation for refractory, disabling symptoms.
Focal dystonias Confined to one part of the body, eg spasmodic torticollis (head
pulled to one side), blepharospasm (involuntary contraction of orbicularis oculi,
OHCS
rarely generalize. They are worsened by stress. Patients may develop a geste
antagoniste to try to resist the dystonic posturing (eg a touch of the finger to
the jaw in spasmodic torticollis). Injection of botulinum toxin into the overactive
muscles is usually eective.
Acute dystonia May occur on starting many drugs, including neuroleptics and
some anti- emetics (eg metoclopramide, cyclizine). There is torticollis (head pulled
back), trismus (oromandibular spasm), and/ or oculogyric crisis (eyes drawn up).
You may mistake this for tetanus or meningitis, but such reactions rapidly disappear after a dose of an anticholinergic, see
deletion). Exclude Wilson’s disease and dopa- responsive dystonia
L
- dopa trial). Anticholinergics and muscle relaxants may help. Deep
p
341
), writer’s cramp. Focal dystonias in adults are typically idiopathic, and
5– 10
yrs. Autosomal dominant inheritance is
p
827
.
St Vitus’ dance
Throughout the Middle Ages, Europe was plagued by epidemics of ‘dancing mania’,
in which aicted individuals were described to have danced wildly, displaying
strange contortions and convulsions until they collapsed from exhaustion. If the
aicted touched a relic of St Vitus they were miraculously cured: observing this,
Paracelsus,
phenomenon of chorea Sancti Viti (‘St Vitus’ dance’). There may have been an infectious component, although mass hysteria induced by religious cults that swept
across medieval Europe seems a more likely cause. Chorea was subsequently used
as a general term for large- amplitude involuntary movements before being further
refined by physicians such as Sydenham (though he did not connect his eponymous
chorea seen in rheumatic fever with an infectious trigger) and Charcot. Nowadays,
a more frequent cause of involuntary movements with behavioural disturbance
is
in Susannah Cahalan’s excellent
Madness. (See also
16
th- century Swiss- German physician and philosopher, described the
NMDA
- receptor antibody encephalitis, the impact of which was documented
BOX
2012
‘S yden ham’s chore a’, p
autobiography Brain on Fire: My Month of
147
.)
465
10 Neurology
10 Neurology
Stroke: acute assessment and management
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466
Infarction or bleeding into the brain manifests with sudden- onset focal
Incidence rates have fallen by
fourth leading cause of death and the largest cause of neurological disability in the
Causes Ischaemic • Cardioembolic (AF; endocarditis; MI— see
• Large artery disease; atherothromboembolism (eg from carotids) or throm-
stroke’).
bosis in situ
Rarer causes Haemodynamic; sudden BP drop by ≥40mmHg (most likely to aect
• Small vessel occlusion/ cerebral microangiopathy. Haemorrhagic (p
the boundary zone between vascular beds), carotid artery dissection (spontaneous, or
from neck trauma or connective tissue disorders), vasculitis, vasospasm (
plasm, venous sinus thrombosis (
Modifiable risk factors BP, smoking, DM, heart disease (valvular, ischaemic, AF),
peripheral vascular disease, combined
Symptoms Ask about: • Exact time of onset of symptoms (use the time defin-
itely last well for ‘wake- up’ strokes); crucial to determine if within the reperfusion
therapy treatment window
exceptions include bleeds and certain
ures with post- ictal paresis (Todd’s palsy), aphasia, or neglect; sepsis; migraine;
intracranial tumours; hypoglycaemia.
Signs Worst at onset. Pointers to bleeding (unreliable!): meningism, severe head-
ache, coma. Pointers to ischaemia: carotid bruit,
50
%) Depending on site there may be contralateral sensory loss or hemiplegia;
(
dysphasia; homonymous hemianopia.
quadriplegia, disturbances of gaze and vision, vertigo, locked- in syndrome (aware,
but unable to respond).
thalamus, and pons. Five syndromes: ataxic hemiparesis, pure motor, pure sensory,
sensorimotor, and dysarthria/ clumsy hand. Cognition/ consciousness are intact except in some thalamic strokes.
Acute investigation and management ‘Time is brain.’
Protect the airway This avoids hypoxia/ aspiration. Check glucose pre- hospital.
• History and exam Establish time of onset (see above), establish severity (
•
CT/ MRI
Without delay if: thrombolysis considered, risk of haemorrhage (
ICP
signs of
, severe headache, meningism, progressive symptoms, bleeding tendency or anticoagulated), or unusual presentation (eg fluctuating consciousness,
fever). Diusion- weighted
• Urgent reperfusion treatment Assess suitability for thrombectomy (see
‘Endovascular thrombectomy’). Consider
as haemorrhage has been excluded, provided the onset of symptoms was
(the benefits outweigh the risks within this window, though best results are
or for ‘wake- up’ stroke with imaging signs of hyperacuity. Alteplase is the agent of
Always do CT 12– 24h post- lysis to identify bleeding. Absolute CI to thromb-
choice.
• Resolved deficit • Any haemorrhage on CT. • Recent surgery, trauma, or ar-
olysis:
tery or vein puncture at uncompressible site.
• Stroke or serious head injury in last 6 weeks. • GI or urinary tract haemor-
(active).
rhage in the last
INR >
1.7
• Admit to an acute stroke unit Multidisciplinary care improves outcomes (p
21
days. • Anticoagulants (if
• Platelets <50 ≈
• Maintain homeostasis Blood glucose: keep between 4– 11 mmol/ L. Blood pres-
sure: only treat within
athy or aortic dissection) or thrombolysis is considered as treating
cerebral perfusion.
• Screen swallow ‘Nil by mouth’ until this is done (but keep hydrated).
• Secondary prevention To be commenced as soon as haemorrhagic stroke is ex-
p
470
cluded (
5
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts & Leucoencephalopathy: the main
genetic cause of stroke (there is also an autosomal recessive form).
6
The best- established deficit rating scale, used to select patients for reperfusion: www.nih stro kesc ale.org.
).
CNS
20
% in the last two decades, but stroke remains the
BOX
‘Cardiac causes of
signs.
468
p
478
), Fabry disease (p
OCP
, lipids, alcohol use, clotting (p
316
),
CADASIL.
5
370
).
p
474
), neo-
• Progression; usually sudden and maximal at onset, but
TIA
s (p
469
). • Features of stroke mimics: seiz-
AF
, past
TIA, IHD
. Cerebral infarcts
Brainstem infarcts (25%) Varied; include
Lacunar infarcts (25%) Basal ganglia, internal capsule,
NIHSS
GCS
MRI
is most sensitive for an acute infarct (fig
IV
thrombolysis in disabling stroke as soon
•
AVM
/ aneurysm or intracranial tumour
INR >
1.7
or a
PTT
109/ L. • Endocarditis or
24
h if there is a hypertensive emergency (eg encephalop-
CNS
>40s), or spontaneous
vasculitis.
10.15
≤
4.5
≤
90
BP
may impair
).
BOX
h ago
min),
470
UK.
).
6
).
,
).
Endovascular thrombectomy: a new era in stroke therapy
CHA2DS2VASC
https://t.me/med1917
Although early reperfusion with thrombolysis is extremely eective, only ¼ of
those with large proximal intracranial vessel occlusion have a good outcome.
Intra- arterial mechanical clot removal has revolutionized care in this group, with
an unprecedented number needed to treat of <
terior circulation events).
CT
angiography or MR angiography should be performed
3
for improved outcomes (for an-
to assess suitability where thrombectomy is available (the main limiting factor is
service provision, typically by interventional radiologists).
Who to refer Acute stroke wit h confir med larg e vessel occ lusion , no ocial severity
6
cut- o especially if the occlusion is proximal, <
anterior events
6– 24
h after careful selection with CT perfusion imaging).4 Procedure
A stent clot retriever is passed via the femoral artery. Usually under conscious sedation rather than general anaesthesia, but evidence is lacking.
15
%; vasospasm, arterial perforation/ dissection, device misplacement.
~
h of symptom onset (beneficial in
Complications In
467
Cardiac causes of stroke
Cardioembolic causes are the source of stroke in >30% of patients. The finding of
infarcts in multiple arterial territories on imaging is particularly suggestive.
Non- valvular atrial fibrillation (p
4.5
%/ yr, and ischaemic strokes in AF carry a worse prognosis.
•
AF
score (p
127
. Oer anticoagulation in patients with a score of 2 or above. Take bleeding
risk into account: calculate the risk of major bleeding using the
Caution and regular review of oral anticoagulants are required if the
3
. Do not oer primary stroke prevention therapy in patients with AF if
score >
65
yrs and
<
• Anticoagulation (p
and
anticoagulant (
Other cardiac sources of emboli • Cardioversion. • Prosthetic valves. • Acute
myocardial infarct with large left ventricular wall motion abnormalities on echocardiography.
emboli’).
20
% of those with endocarditis present with
CHA2DS2VASC
346
7
days after a major stroke, and immediately after
DOAC
).
• Patent foramen ovale/ septal defects (stroke cause by ‘paradoxical
• Cardiac surgery. • Infective endocarditis (gives rise to septic emboli;
126
) Associated with an overall risk of stroke of
) can be used to calculate risk of stroke in patients with
HAS- BLED
score.
HAS- BLED
score is 0 for men or 1 for women.
) commence within 48h after a minor or moderate stroke
TIA
. Oer a direct oral
CNS
signs).
10 Neurology
Fig 10.
15
The T2- weighted (p
Dierentials: infarct (right
right shows restricted diusion in the region, suggesting this is an infarct.
PCA
730
) image on the left shows oedema in the right occipital lobe.
), inflammation, or tumour. The diusion- weighted image on the
© Prof Peter Scally.
10 Neurology
Intracerebral haemorrhage (
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468
ICH
)
Bleeding within the brain parenchyma (versus intracranial haemorrhage, which
p
478
, p
476
).
ICH
refers to any bleeding within the cranial vault,
common form of stroke (accounting for
fatality rate is
40
% and <50% survive 1 year. Therapeutic nihilism is rife because
15
%) and the most severe. The 1- month case
is the second most
of these harrowing statistics, but evidence in favour of aggressive management is
amassing and undue care- limiting decisions in the early stages worsen outcomes.
Oer full supportive care & postpone
DNR
orders until at least 24– 48h in most cases.
Symptoms/ signs Similar presentation to ischaemic stroke, but features of mass
eect (headaches, vomiting, decreased level of consciousness, seizures) due to the
haematoma are more suggestive of
Causes Traumatic
mainder in the absence of trauma or surgery are termed ‘spontaneous’.
small vessel disease (
ICH
is by far the most common type and easily identified; the re-
85
%) rupture of small vessels damaged by hypertension or
amyloid angiopathy (amyloid protein deposition in cortical arterioles)
macrovascular or neoplastic cause (
cavernomas (
fig
10.16
), aneurysms, venous thrombosis.
Diagnosis Acute evaluation as for ischaemic stroke (p
CT
(fig
made on plain
10.16
there is a suspicion of a macrovascular cause, +
ICH
.
20
%) eg arteriovenous malformations,
). Perform vascular imaging (
MRI
and formal angiography if –ve.
466
); the diagnosis is readily
CT/ MR
angiography) when
Specific management General principles of acute management are the same as
p
for ischaemic stroke, including multidisciplinary stroke unit care (
• Anticoagulation/ antiplatelet therapy associated bleeds Stop the oending
466
agent in the short term. Reversal agents for anticoagulation should be administered as soon as possible (prothrombin complex concentrate for warfarin, specific reversal drugs for direct oral anticoagulants, eg andexanet alfa for factor Xa
inhibitors, idarucizumab for dabigatran).
• Acute BP lowering IV antihypertensive treatment (eg labetalol,
tients with systolic
• Referral for neurosurgery Rapidly deteriorating patients with risk of brainstem
compression from cerebellar
ation/ decompression. For patients with supratentorial
niotomy is recommended in some deteriorating, but not stable, patients. External
BP
>
150
and symptom onset <6h, targeting
ICH
should be referred for urgent surgical evacu-
130– 140
ICH
, early referral for cra-
ventricular drain insertion is oered for hydrocephalus, especially in the context
of intraventricular extension/ primary intraventricular haemorrhage.
Complications Haematoma expansion; seizures; perihaematomal oedema; hydro-
cephalus; hyperglycaemia; venous thromboembolism. Surveillance and early management is critical.
(a) (b)
• Cerebral
• Underlying
), but consider:
GTN
) for all pa-
mmHg.5
Fig 10.
16
The axial pl ain CT (a) shows an acute large right temporoparietal primary
some eacement of the right lateral ventricle. The
cavernoma with intracapsular haemorrhage (secondary
T2
- weighted
MRI
ICH
(b) shows a left thalamic
). © Iain McGurgan.
ICH
with
Transient ischaemic attack (
https://t.me/med1917
TIA
)
Temporary focal neurological symptoms caused by cerebral, retinal, or spinal cord
ischaemia, without infarction. About
% of stroke patients report a preceding
TIA
20
Without intervention, 1 in 10 will go on to have a stroke within a week, so emer-
gency investigation and management is imperative; all patients should be seen
24
hours of onset of symptoms.
within
Symptoms/ signs Abrupt onset of maximal symptoms specific to the arterial terri-
p
446
tory involved (
ally last <
unilateral progressive vision loss ‘like a curtain descending’. Attacks may be single or
many; multiple highly stereotyped attacks (‘crescendo’
nial stenosis (commonly the superior division of the
); these should be the same as known stroke syndromes.
1
hour. Amaurosis fugax occurs when the retinal artery is occluded, causing
TIA
S) suggest a critical intracra-
MCA
) or recurrent lacunar events
TIA
S usu-
due to disease of an internal capsule penetrating artery (‘capsular warning syndrome’).
Causes (As causes of ischaemic stroke, see p
TIA
S have the highest risk of early stroke.
Dierentials Over a half of
approach runs the risk of dismissing the not infrequent chameleons. Hypoglycaemia,
migraine aura (
clude twitching and jerking), hyperventilation, retinal bleeds can mimic
p
454
TIA
clinic referrals are mimics, but an overly dogmatic
), focal epilepsy (symptoms spread over seconds and often in-
events (eg syncope, dizziness, amnesia) are not typical of
amic or brainstem ischaemia can cause loss of consciousness. Limb- shaking
can occur in hemispheric hypoperfusion due to severe large artery stenosis.
mimics of
TIA
Malignant hypertension, MS (paroxysmal dysarthria), intracranial
466
.) Large- artery disease- induced
TIA
TIA
S, but transient thal-
. Global
TIA
Rare
tumours, peripheral neuropathy, phaeochromocytoma, somatization.
Tests Routine CT is not recommended5 in suspected
resolved), unless there are clinical features suggesting
injury, headache, anticoagulation use, repetitive stereotyped events). Diusion-
MRI
weighted
for endarterectomy is a possibility) are performed in the
± vascular imaging (
CT/ MR
angiography, or carotid Doppler if referral
diagnosis and establish the territory and cause if necessary. Blood tests and cardiac
investigations as in the assessment of ischaemic stroke (
Treatment Advise aspirin
required first to investigate for an alternative cause, as above) and refer urgently to
TIA
clinic. Once the diagnosis is confirmed:
the
• Antiplatelet drugs Recent trial evidence supports acute dual antiplatelet therapy in
TIA
and minor stroke.6 Commence aspirin & clopidogrel (both 75mg OD, in the place
300
of aspirin
• Anticoagulation indications Stop antiplatelet treatment and start anticoagulation
if a cardioembolic source is confirmed (
• Urgent carotid endarterectomy Perform within 2wks of first presentation if
there is
mg if already started), switching to clopidogrel alone after 10– 21 day s.
70– 99
% stenosis,7 the symptoms are referable to the carotid artery dis-
300
mg daily immediately in suspected cases (unless CT is
p
467
).
tribution, and operative risk is acceptable (higher risk in: , >
TIA
(where symptoms have
ICH
or another cause (head
TIA
clinic to confirm the
p
466
).
75
yrs, systolic BP,
contralateral artery occluded; ipsilateral carotid syphon/ external carotid stenosed). Do not stop aspirin preoperatively. Surgery is preferred to endovascular carotid artery angioplasty with stenting in those fit enough to tolerate due to higher
peri- procedure stroke and mortality rates with stenting.
• Commence other secondary prevention (See p
Driving Prohibited for at least 1 month, see p
Prognosis Risk of recurrent stroke in the 3 months after
with early initiation of secondary preventive treatment. Long- term risk of stroke or
cardiovascular events following
artery disease and cardioembolic
TIA
S is dependent on the aetiology (worse for large-
TIA
) underlying vascular risk factors.
150
470
.)
.
TIA
is reduced by 80%
469
.
10 Neurology
s
7
Interventions for 50– 69% stenoses can be justifiable; individualize risk and check local guidelines. In particular, check which criteria used to estimate degree of stenosis since
Carotid Endarterectomy Trial) criteria tend to include some more severe lesions in
pared to the
ECST
(European Carotid Surgery Trialists’ Collaborative Group) criteria.
NASCET
(North American Symptomatic
50– 69
% range as com-
470
10 Neurology
https://t.me/med1917
Stroke and
TIA
: prevention
More than 1 in 4 people with stroke have had a previous stroke or
Primary prevention (Ie before any
Control risk factors (p
cardiac disease (see
p85). Exercise helps (
(
AF
(see
BOX
‘Cardiac causes of stroke’, p
466
BOX
‘Cardiac causes of stroke’, p
HDL
TIA
/ stroke.)
): look for and treat hypertension, DM, lipids (p
467
) and help quit smoking
, glucose tolerance). Use lifelong anticoagulation in
467
) and prosthetic heart valves.
Secondary prevention (Ie preventing further strokes.) Accurate diagnosis of
TIA
/ stroke subtype (see causes of ischaemic stroke, p
466
) is crucial for deter-
mining the best secondary prevention approach.
Perform further testing (See p
the subtype and risk factors for further strokes. Look for:
• Hypertension. Check blood pressure and consider home or ambulatory measurement.
• Cardiac source of emboli. (See
AF
(p
126
look for
), and more prolonged monitoring if this is negative but imaging
is suggestive of a cardioembolic source. Echocardiogram may reveal an enlarged
left atrium, mural thrombus due to
MI
. It may also show valvular lesions in infective endocarditis, rheumatic
post-
466
for imaging.) Investigate promptly to identify
BOX
‘Cardiac causes of stroke’, p
AF
, or a hypokinetic segment of cardiac muscle
heart disease, or atrial septal abnormalities (bubble study). Transoesophageal
echo is more sensitive than transthoracic.
• Carotid artery stenosis. Do carotid Doppler US ±
Benefits and risks of revascularization should be individualized by an expert but
generally most with ≥
some (especially ) will benefit with
• Hypoglycaemia, hyperglycaemia, dyslipidaemia, and hyperhomocysteinaemia.
• Vasculitis.
• Prothrombotic states, eg thrombophilia (p
ESR, ANCA
• Hyperviscosity, eg polycythaemia (p
• Thrombocytopenia and other bleeding disorders.
• Genetic tests.
70
% stenosis and life expectancy ≥5yrs will benefit while
50– 69
(p
554
).
VDRL
to look for active, untreated syphilis (p
362
), sickle cell disease (p
CADASIL
(p
466
); Fabry disease (p
CT/ MRI
angiography (fig
% stenosis (p
370
), antiphospholipid syndrome (p
469
).
336
316
).
Commence secondary prevention treatment
• Antihypertensive treatment. Elevated BP is the strongest modifiable risk factor
BP
for stroke, and in stroke survivors,
events independently of the baseline
24– 48
therapy
target a
• Control modifiable risk factors. (As ‘Primary prevention’.)
• Antiplatelet agents. (See
mary haemorrhage on
hours after major stroke and immediately after minor stroke/
BP
of <
130
/ <80mmHg.
CT
, give 2 weeks of aspirin
clopidogrel monotherapy. If this is
lowering reduces recurrent cerebrovascular
BP.
Initiate (or reinstate) antihypertensive
BOX
‘Antiplatelets’, and
CI
or not tolerated then give low dose aspirin
TIA
treatment, p
300
mg, then switch to long- term
plus slow- release dipyridamole (equally eective but dipyridamole has a poorer
side eect profile).
• Anticoagulation. Commence in cardioembolic stroke; relative risk reduction of
recurrent stroke of
• Cholesterol- lowering treatment. Commence high- dose statin treatment
(atorvastatin
• Patent foramen ovale closure. Percutaneous transcatheter device closure is more
eective than medical therapy alone in cryptogenic cases (stroke with no established cause), at least in those aged ≤
Prognosis Overall mortality: 38
Age, stroke severity, and the aetiology (worst for cardioembolic and large artery)
are the biggest predictors of prognosis. Avoid pressure ulcers (
60
% (see
BOX
‘Cardiac causes of stroke’, p
80
mg first line, if tolerated) regardless of baseline
60
yrs.7
000
/ yr in the UK, 1 in 8 are fatal within 1 month.
467
fig
TIA.
467
).
469
).
LDL
10.18
.) 24h
408
.) If no pri-
.
).
ECG
10.17
).
552
TIA
682
),
to
).
).
to
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