Vascular Neurosurgery Flashcards

(223 cards)

1
Q

Name the labelled structures

A

A- left vertebral artery

B- Right vertebral artery

C- Right anterior inferior cerebellar artery (AICA)

D- Basilar artery

E- Superior cerebellar artery

F- Left posterior cerebral artery

G- Arrowhead on R ICA.

H- L ICA

I- L ICA bifurcation into ACA and MCA

J- Left ACA

K- Left MCA

L- ACA

M- AComm

N- Bifurcation of R MCA

The PICA normally branches off the distal part of the vertebral arteries

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2
Q

A 64-year-old man presented to the emergency department after experiencing a severe headache which began suddenly when he was watching TV. He felt nauseous and had vomited several times. At hospital, his GCS was 14/15 (E3, V5, M6), and his pupils were equal and reactive, with no focal neurological deficits. He had a history of hyper- tension and his blood pressure was 181/122mmHg.

What is the differential diagnosis, and what investigation should be performed?

A

The differential diagnosis for a severe sudden onset headache includes any variety of intracranial haemorrhage (subarachnoid haemorrhage (SAH), intracerebral haemorrhage, pituitary apoplexy) and migraine. Intracerebral haemorrhage is usu- ally accompanied by lateralizing signs. A CT scan should be performed urgently to exclude intracranial haemorrhage.

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3
Q

What is the diagnosis

Identify the arrowed features on the scan

A

SAH with evidence of hydrocephalus

  1. Blood in sulci

2 + 3: Frontal and occipital horns of the lateral ventricles are dilated as is the third ventricle (4)

There is intraventricular blood (5)

The low-denstry area around the frontal horn represents transependymal flow (6) due to acute hydrocephalus

Blood is seen in the right sylvian fissure, 7, and in the interpeduncular cistern, 8 and the right and left, 9 10, ambient cisterns.

The quadrigeminal cistern 11 is clear of blood.

The temporal horns of the lateral ventricles are dilated

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4
Q

What are the causes of SAH

A

Trauma

Spontaneous SAH:

Ruptured cerebral aneurysm (70% of cases)

AVM (5-10%)

Vasculitis- e.g. SCD or moyamoya disease

In 15-20% of patients, all investigations including catheter angiography prove negative

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5
Q
A

In this case the asymmetrical blood distribution is highly suspicious of a ruptured aneurysm on the right middle cerebral, posterior com- municating or internal carotid artery

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6
Q

What are the general measures that need to be instituted for a patient with aneu- rysmal subarachnoid haemorrhage, and what are the specific management issues in this case?

A

Supportive- optimise cerebral perfusion

Identify the aneurysm and secure it.

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7
Q

General measures in Mx of SAH

A

Mx in HDU or ICU setting with frequent neuro-obs

Bed rest to minimise fluctuations in BP

Bloods- FBC, electrolytes, clotting, G+S

Analgesia- paracetamol and codeine

Laxatives to reduce straining

DVT prophylaxis with TEDS (LMWH after surgical mx of aneurysm)

Adequate hydration to reduce risk of volume depletion

CXR to exclude neurogenic pulmonary oedema

ECG to detect myocardial damage

Nimodipine for 21/7.

Specific measures to improve cerebral perfusion e,.g. CSF diversion or haematoma evacuation to reduce ICP.

Cerebral angiography to look for aneurysm

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8
Q

Mx of BP in SAH

A

Patients with SAH often present with raised BP.

The risk of aneurysm rupture should be balanced against the risk of cerebral hypoperfusion.

BP should not be aggressively managemend in the acute setting.

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9
Q

Mx of hydrocephalus in SAH

A

Immediate CSF diversion

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10
Q

Options for CSF diversion

A

LP

Lumbar drain

External ventricular drain

(First two are relatively contraindicated in the presence of mass effect or obstructive hydrocephalus)

LP carries lower morbidity.

EVD may be preferrable if there is a high blood load to allow controlled drainage of CSF and if there is intraventricular blood which could block CSF flow through the ventricles.

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11
Q
A

A- ICA

B- Ophthalmic

C- ACA, A1 segment

D- MCA, M1 segment

E- aneurysm

F- ACA, A2 segment

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12
Q

What are the different patterns of bleeding in aneurysmal SAH

A

A Sylvian fissure

B Basal cisterns

C Interhemispheric, frontal lobe

D Intraventricular

E Subdural

F Perimesenecephalic

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13
Q

Location of blood- predictiveness of aneurysm site

A

Location of blood is predictive of site of ruptured aneurysm in around 80% of SAH patients.

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14
Q

Perimesencephalic SAH

A

Presents as typical SAH but usually less distressed and neurologically disabled.

Angiography is usually normal and bleed is usually considered to be venous e.g. pontine vein

Requiring no further treatment

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15
Q

SAH aneurysm location by site of bleeding:

Sylvian fissure

A

MCA

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16
Q

SAH aneurysm location by site of bleeding:

Basal cisterns

A

Basilar artery, SCA, PCom

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17
Q

SAH aneurysm location by site of bleeding:

Interhemispheric. Frontal lobe

A

ACom, ACA

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18
Q

SAH aneurysm location by site of bleeding:

Intraventricular

A

ACom (through lamina terminalis)

Basilar artery (through 3rd ventricle)

PICA (through 4th ventricle)

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19
Q

SAH aneurysm location by site of bleeding:

Subdural

A

PCom, ACom (through arachnoid)

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20
Q

SAH aneurysm location by site of bleeding:

Perimesencephalic

A

Non arterial e.g. pontine veins

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21
Q

What are the two commonly used scales for SAH grading

A

Fisher grading (Modified fisher)

WFNS

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22
Q

Features of Fisher grading

A

Use the amount of blood seen on CT to predict the subsequent risk of radiological vasospasm.

1-4.

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23
Q

Issues with original Fisher grading

A

Used an early CT scanner with images printed on films. Measured manually with rulers, theefore measurements only apply to images obtained on scanner.

Patients could also be classified into more than one grade

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24
Q

Fisher 1

A

No blood on CT scan

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25
Fisher 2
Diffuse or thin layer of blood with all vertical layers \<1mm thick
26
Fisher 3
\>1mm in vertical fissures or cisterns/localised clot
27
Fisher 4
Diffuse or no subarachnoid blood but with intracerebral or intraventircular clots
28
Modified Fisher 0
No blood
29
Modified Fisher 1
Focal or diffuse thin SAH, no IVH
30
Modified Fisher 2
Focal or diffuse thin SAH with IVH
31
Modified Fisher 3
Focal or diffuse thick SAH with no IVH
32
Modified Fisher 4
Focal or diffuse thick SAH with IVH
33
WFNS grading of SAH
Based on GCS
34
WFNS 1
GCS 15
35
WFNS 2
GCS 13-14 with no focal neurology
36
WFNS 3
GCS 13-14 with focal neurological deficit
37
WFNS 4
GCS 7-12
38
WFNS 5
GCS 3-6
39
Coiling vs Clipping Trial
ISAT demonstrated that for a selected population (good grade, M/ACA suitable for both coiling and clipping) Coiling associated with lower risk of dependency or death at 1y. Difference not seen at 5y
40
Features of cerebral aneurysm favouring coiling
Posterior circulation aneurysm- difficult access Poor-grade patients Elderly Presence of medical comorbidities Raised ICP
41
Features of aneurysm favouring clipping
Wide necked aneurysm Aneurysm incorporating branching arteries Coexisting haematoma requiring evacuation Acute brainstem compression
42
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. Explain the clinical signs.
This patient has left III nerve palsy.
43
CN III motor portion
Supplies LPS and extraocular muscles except LR and SO
44
Parasympathetic portion of CN III
Innervate the sphincter pupillae muscle in iris
45
Consequence of CN III denervation
Ptosis, mydriasis and down (unopposed SO) and out (unopposed LR) pupil
46
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. DDx?
DDx includes any lesion affect CN III. History sudden onset headache, the priority is to exclude SAH from an aneursym compressing the third nerve. Another less common cause of III palsy is pituitary apoplexy
47
How does CN III palsy occur in pituitary apoplexy
The intracavernous segment of the third nerve is compressed by the expanding pituitary mass.
48
Sensitivity of CTH for blood in the first 24h after SAH?
95% Reduces to 70% after 3 days. After 6d, a CT scan is not sensitive enough to detect an SAH
49
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. CTH was done and is shown. What does it show? What should be done?
It is a normal CTH LP to exclude SAH may be reasonable. An alternative would be to proceed directly to cerebral angiography as an aneurysm, if found, will require urgent treatment in this context, whether or not it has bled given it is symptomatic
50
When should LP be performed for ?SAH
Timing depends on which diagnostic test is used. Spectrophotometry rests on the detection of bilirubin and should be performed after 12h
51
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. How should this patient be managed whilst she awaits the results of the LP?
She should receive standard medical treatment for SAH pending the results.
52
A- ICA B- Ophthalmic C- PCA D- Anterior choroidal artery E- Anterior cerebral artery F- aneurysm which arises from posterior communicating artery
53
How can a PCA aneursym cause a third nerve palsy?
The paired oculomotor nerves exit the midbrain anteriorly. They lie between the PCA above and the superior cerebellar artery below, either side of the basilar artery. They then pass forward via the lateral wall of the cavernous sinus to enter the orbit via the SOF. CN III passes by the point where the PCA branches off the internal carotid. The site of origin of most PCA aneurysms.
54
What other aneursysm can cause CN III palsy?
PCA Superior cerebellar artery Basilar tip
55
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. The patient underwent coil embolization of the aneurysm. The post-procedure angiogram shows obliteration of the aneurysm The patient makes a good recovery and returns to the ward with no neurological deficits. Twelve hours later, you are informed that the patient has deteriorated. On examination, the patient is drowsy, and her GCS is 11/15 (E3, V3, M5). (a) What are the common causes of deterioration in this scenario?
Common causes for neurological deterioration after SAH: Re-bleed from aneurysm (unlikely in this case as the aneurysm has been secured) Vasospasm Hyponatraemia Hydrocephalus Seizures Hospital-acquired infections
56
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. The patient underwent coil embolization of the aneurysm. The post-procedure angiogramshows obliteration of the aneurysm The patient makes a good recovery and returns to the ward with no neurological deficits. Twelve hours later, you are informed that the patient has deteriorated. On examination, the patient is drowsy, and her GCS is 11/15 (E3, V3, M5). b) How should this patient be managed?
ABC Urgent CT scan Blood test to include electrolytes and inflammatory markers. Adequate hydration should be ensured as dehydration increases the risk of vasospasm.
57
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. The patient underwent coil embolization of the aneurysm. The post-procedure angiogram shows obliteration of the aneurysm The patient makes a good recovery and returns to the ward with no neurological deficits. Twelve hours later, you are informed that the patient has deteriorated. On examination, the patient is drowsy, and her GCS is 11/15 (E3, V3, M5). CT scan is shown below. Describe appearances:
Blood is seen in the interhemispheric fissure (A), both Sylvian fissures, left (B) more than the right (C) and both ambient cisterns (D). There is hydrocephalus indicated by enlargement of the temporal horns of the lateral ventricles (E) and the third ventricle (F)
58
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. The patient underwent coil embolization of the aneurysm. The post-procedure angiogram shows obliteration of the aneurysm The patient makes a good recovery and returns to the ward with no neurological deficits. Twelve hours later, you are informed that the patient has deteriorated. On examination, the patient is drowsy, and her GCS is 11/15 (E3, V3, M5). What has happened? What should be done now?
The presence of subarachnoid blood confirms the patient has re-bled as the admission was normal. This may have occurred from the aneurysm that was treated or from a separate aneurysm that was not identified on initial imaging. The patient should have urgent repeat angiography to determine whether the treated aneurysm is secure and to look for additional aneurysms. The repeat angiogram in this patient showed that the treated aneurysm was apparently secure and no additional vascular abnormalities were demonstrated. The patient proceeded to a craniotomy and a small remnant of the aneurysm neck, which was not seen on angiography, was found. This was clipped.
59
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. The patient underwent coil embolization of the aneurysm. The post-procedure angiogramshows obliteration of the aneurysm The repeat angiogram in this patient showed that the treated aneurysm was apparently secure and no additional vascular abnormalities were demonstrated.The patient proceeded to a craniotomy and a small remnant of the aneurysm neck, which was not seen on angiography, was found. This was clipped. The day after surgery, you are alerted as the patient has developed left sided weakness. On examination, the patient is drowsy with a GCS of 11/15 (E3, V3, M5). There is partial ptosis of the left eyelid. The pupils are both reactive; the left is size 4 and the right is size 3. There is grade 4/5 weakness in the left arm and leg. What are the potential causes of deterioration?
The causes of neurological deterioration listed previously apply to any deteriorating patient with SAH. However, the presence of lateralizing signs in this scenario make hyponatraemia, hydrocephalus, and hospital-acquired infections relatively less likely. Additionally, a postoperative haematoma requires consideration in this scenario as the patient has just had a craniotomy, and an urgent CT scan should be performed to exclude this.
60
A 49-year-old woman presented to hospital having suffered a sudden-onset severe headache 6 days previously. She felt nauseous at the time of the headache, although she did not vomit. The headache reached maximum intensity 24 hours after onset and then eased, but has persisted. Three days prior to admission she noticed that her left eyelid was drooping. She attended her general practitioner who arranged for her to be seen in the emergency department. On examination, she was alert and orientated (GCS 15/15). Her left eyelid was closed and she could not open it. When the eyelid was lifted, the left pupil was dilated and the eye was found to be looking down and out. No other neurological deficits were found. The patient underwent coil embolization of the aneurysm. The post-procedure angiogramshows obliteration of the aneurysm The repeat angiogram in this patient showed that the treated aneurysm was apparently secure and no additional vascular abnormalities were demonstrated.The patient proceeded to a craniotomy and a small remnant of the aneurysm neck, which was not seen on angiography, was found. This was clipped. The day after surgery, you are alerted as the patient has developed left sided weakness. On examination, the patient is drowsy with a GCS of 11/15 (E3, V3, M5). There is partial ptosis of the left eyelid. The pupils are both reactive; the left is size 4 and the right is size 3. There is grade 4/5 weakness in the left arm and leg. The patient has a CT scan which shows no new changes. What is the diagnosis? Mx?
CT scan excludes post-operative haematoma and re-bleed. Likely diagnosis is delayed cerebral ischaemia due to vasospasm Treatment strategies are controversial and vary but have been traditionally based on volume resuscitation and induced hypertension.
61
Def: vasospasm
Spasm or narrowing of the cerebral vasculature that may follow SAH. It is often seen in aneurysmal SAH but rare in non-aneurysmal SAH (including traumatic SAH, perimesencephalic SAH and SAH from vascular malformations).
62
Pathophysiology of vasospasm
Not clearly established though various endothelial mediators are thought to play a role
63
In what proportion of patients with aneursymal SAH is radiological vasospasm seen?
70% and may or may not lead to a clinically detectable neurological deficit
64
Describe the image shown
AP right internal carotid angiogram on admission (left) and after 4 days with evolving left hemiparesis (right) of a 41-year-old man with a subarachnoid haemorrhage. By day 4 there is severely reduced calibre of the terminal internal carotid artery which begins just proximal to the aneurysm (A, transition point; B, aneurysm). The proximal MCA (C) and ACA (D) are both very severely attenuated compared with the earlier angiogram. This is diagnostic of severe vasospasm
65
What is meant by the terms delayed cerebral ischaemia (DCI), delayed ischaemic neurological deficit (DNID) or symptomatic vasospasm
Used when vasospsm leads to a clinical neurological deficit
66
What proportion of patients with aneurysmal SAH are affected by symptomatic vasospasm?
30%
67
When does cerebral vasospasm typically occur after SAH?
7-14d after ictus but may be up to 21/7 after haemorrhage. The deficit may be permanent if cerebral infarction occurs.
68
What is the only intervention that has been shown to improve the outcome associated with DCI?
Administration of 60mg oral nimodipine every 4 hours, reduced the risk of cerebral infarction by 34% and poor outcomes by 40%
69
Pickard et al 1989
Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. Showed reduction in incidence of cerebral infarction by 34% Reduction in poor outcomes by 40%
70
What is the main approach to therapy when DCI occurs?
The overall goal is to augment cerebral blood flow to the affected area Triple H therapy
71
Triple H therapy
Haemodilution Hypertension Hypervolaemia
72
Approach to triple H therapy
Adequate hydration, which can be gauged by CVP monitoring. Inotropes to augment MAP. Endovascular therapies such as transluminal angioplasty and intra-arterial release of vasodilators have not been proved in RCTs but may be used in refractory cases.
73
Oblique muscles and eye movements.
The oblique muscles principally act when the eyeball is turned medially whereas the superior and inferior rectus muscles generally work when the eye is turned laterally.
74
The affected eye looks ‘down and out’ in the resting position due to the unopposed action of the lateral rectus and superior oblique. There would also be ptosis and the pupil will be fixed and dilated
Oculomotor (III)
75
The affected eye looks up and slightly medially in the resting position. Diplopia is maximal when the patient looks ‘down and in’. Tilting the head to the unaffected side attenuates the diplopia and some patients may adopt this posture.
Trochlear (IV)
76
The resting position may be normal although the affected eye may be looking slightly medially. The patient is unable to abduct the affected eye. Diplopia is maximal on horizontal gaze in the direction of the affected eye, and the patient may compensate by turning the head in the direction of maximal diplopia.
Abducens (VI)
77
RBCs in LP in SAH
Number of RBCs in CSF will be uniformly raised in all bottles. A decreasing number in sequential bottles is more consistent with traumatic tap. Although the patient may also have had an SAH
78
Absolute number of RBCs in LP in SAH
If the red cell count is only mildly elevated (hundreds), SAH is less likely as the RBC count in SAH is usually in the thousands
79
Features of xanthochromia
The CSF is inspected after it has been centrifuged. The result is positive if it has an orange tinge (the sample is held against a white background). A traumatic tap may also produce a positive result.
80
Sensitivity and specificity of xanthochromia in SAH
93% , a specificity of 95% , a positive predictive value of 72% , and a negative predictive value of 99%
81
Features of spectrophotometry
Differentiates between SAH and traumatic tap by detecting oxyhaemoglobin and bilirubin in the CSF. Any blood that enters the CSF (from SAH or truamatic tap) will convert to oxyhaemoblogin as this occurs both in vivo and in vitro. In contrast the breakdown of RBCs into bilirubin only occurs in vivo and takes at least 12h and thus cannot result from a traumatic tap. Therefore a CSF sample taken 12h after headache onset that is positive for bilirubin is consistent with SAH. High CSF protein or serum bilirubin may also result in raised CSF bilirubin.
82
Additional Ix in ?SAH
If in any doubt- angiography. Vasospasm which suggests recent haemorrhage can also be detected. Alternatively MRI with gradient echo and MRA sequences can demontsrate the presence of blood and aneurysm.
83
A 48-year-old man was found collapsed at work. He cried out briefly and then fell to the floor. He was seen to shake and stop breathing for a short period, and he was taken to hospital immediately. On arrival in the emergency department he was comatose, flexing with the left arm, and localizing with the right. He was snoring and not making any sounds. His pupils were sluggishly reactive to light and his blood pressure was 200/110mmHg. Likely dx?
DDx includes cardiac events, hypoxic brain injury Seizure activity suggests intracerebral event. He may have had a seizure and currently be post ictal though ICH must be excluded
84
A 48-year-old man was found collapsed at work. He cried out briefly and then fell to the floor. He was seen to shake and stop breathing for a short period, and he was taken to hospital immediately. On arrival in the emergency department he was comatose, flexing with the left arm, and localizing with the right. He was snoring and not making any sounds. His pupils were sluggishly reactive to light and his blood pressure was 200/110mmHg. Initial Mx
1o survey IV access, bloods, ECG. Unless it is certain that he is improving neurologically after a seizure, he is likely to require intubation for safe ongoing management including transfer to CT.
85
Troponin and ECG abnormalities in ICH (esp SAH)
Frequently see trop rise/ECG abnormalities Very rarely reflects primary coronary event but rather the sudden myocardial stress caused by an extreme surge in SNS associated with the ictus of SAH
86
A 48-year-old man was found collapsed at work. He cried out briefly and then fell to the floor. He was seen to shake and stop breathing for a short period, and he was taken to hospital immediately. On arrival in the emergency department, he was comatose, flexing with the left arm, and localizing with the right. He was snoring and not making any sounds. His pupils were sluggishly reactive to light and his blood pressure was 200/110mmHg. Mx of BP
BP may be raised in the context of chronic HTN or part of the autoregulation response. It should not be aggressively controlled in the acute setting. Anaesthetic may cause a drop in BP. Efforts to control BP using conventional antihypertensives should be deferred unless his BP settles at an unacceptable level, usually \>200mmHg
87
A 48-year-old man was found collapsed at work. He cried out briefly and then fell to the floor. He was seen to shake and stop breathing for a short period, and he was taken to hospital immediately. On arrival in the emergency department he was comatose, flexing with the left arm, and localizing with the right. He was snoring and not making any sounds. His pupils were sluggishly reactive to light and his blood pressure was 200/110mmHg. He is intubated and CT scanned (shown) What is the likely aetiology
3 key findings: Diffuse SAH in keeping with an aneurysmal haemorrhage Large ICH arising in the left sylvian fissure extending into the temporal lobe. There is no midline shift and the ventricles are symmetrical. There is hydrocephalus Left sylvian fissure haemorrhage is highly suggestive of ruptured left MCA aneurysm
88
What is the usual location of MCA aneurysm
Usually arises at the junction between the proximal MCA (M1) and the first branches (M2).
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Anatomy of the MCA
The proximal MCA is M1 This usually splits into two branches- M2 a bifurcation. One of which then splits into two itself. Occasionally all three M2 branches arise from M1 (a trifurcation)
90
A 48-year-old man was found collapsed at work. He cried out briefly and then fell to the floor. He was seen to shake and stop breathing for a short period, and he was taken to hospital immediately. On arrival in the emergency department he was comatose, flexing with the left arm, and localizing with the right. He was snoring and not making any sounds. His pupils were sluggishly reactive to light and his blood pressure was 200/110mmHg. He is intubated and CT scanned (shown) What are his SAH grades?
This man is a poor grade SAH His WFNS grade is 4 His Modified Fisher grade is 4 His Hunt and Hess grade is also 4
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What is the significance of poor grade SAH
All of the grades have been shown to correlate with worse outcome in terms of death and major disability. The risk of vasospasm and ischaemia leading to irreversible stroke is higher Their complication rate from VAP, DVT and infection is also higher. Treatment to secure aneurysm may also be more challenging as endovascular surgery may be limited by vasospasm. Surgery to clip the aneurysm often finds a swollen brain, making clipping without resection of brain impossible.
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A 48-year-old man was found collapsed at work. He cried out briefly and then fell to the floor. He was seen to shake and stop breathing for a short period, and he was taken to hospital immediately. On arrival in the emergency department he was comatose, flexing with the left arm, and localizing with the right. He was snoring and not making any sounds. His pupils were sluggishly reactive to light and his blood pressure was 200/110mmHg. He is intubated and CT scanned (shown) What is the priorty of management in this patient?
Management of the hydrocephalus. This should be undertaken as soon as possible with EVD Neurological state must then be reassessed with weaning of sedation
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What is an issue with WFNS and Hunt and Hess grading systems
They do not distinguish between coma due to high blood load and coma due to hydrocephalus.
94
Discuss the findings of the CTA in this gentleman with large SAH
There is a left MCA aneurysm. Smaller unruptured AComm aneurysm, There is diffuse vasospasm causing attenuation of the visualised anterior circulation settings bilaterally.
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When should the left MCA aneurysm which has recently bled be treated in this gentleman?
Should be secured ASAP to reduce the risk of re-bleed which is likely to be fatal. Surgery will be challenging and may itself pose an unacceptably high risk. Coiling is likely to be lower risk procedure though there is a much higher chance of recurrence of MCA aneurysm with coiling as the neck cannot be completely secured
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Hunt and Hess grading system
Clinical grading system to grade the severity of SAH
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Hunt and Hess 1
Asymptomatic, mild headache, slight nuchal rigidity
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Hunt and Hess 2
Moderate to severe headache, nuchal rigidity. No neurological deficit other than CN palsy
99
Hunt and Hess 3
Drowsiness/confusion, mild focal neurologic deficit
100
Hunt and Hess 4
Stupor, moderate-severe hemiparesis
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Hunt and Hess 5
Coma, decerebrate posturing
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A 49-year-old woman presented to the emergency department with a one-week his- tory of severe headache. The onset was sudden. It did not cause her to lose conscious- ness although she vomited once. Since then her headaches had continued, and they were so severe that she had been unable to leave the house for 3 days. She had been taking paracetamol and codeine analgesia to little effect. Her medical history was unremarkable but she had smoked 20 cigarettes daily since her teens. On examination she was alert and orientated and the neurological examination was unremarkable. She had no papilloedema. The physicians arranged a head CT scan following which she was referred to neurosurgery. What are the arrowed abnormalities (Fig. 20.1) and suggested management?
There are two areas of hyperdenisty in the sylvian fissures bilaterally. SAH is possible given the history and these would be suspicious for MCA aneurysms. It is also possible that the aneurysms have not bled and there is another cause for her headache. An LP would be reasonable to establish whether she has suffered an LP. This is important as it informs how she should subsequently be managed if an aneurysm is confirmed
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A 49-year-old woman presented to the emergency department with a one-week his- tory of severe headache. The onset was sudden. It did not cause her to lose conscious- ness although she vomited once. Since then her headaches had continued, and they were so severe that she had been unable to leave the house for 3 days. She had been taking paracetamol and codeine analgesia to little effect. Her medical history was unremarkable but she had smoked 20 cigarettes daily since her teens. On examination, she was alert and orientated and the neurological examination was unremarkable. She had no papilloedema. The physicians arranged a head CT scan following which she was referred to neurosurgery. Her LP confirmed SAH. A CT angiogram was arranged and representative images from the maximum intensity projection (MIP) images are shown. What is seen in Fig. 20.2, and what therapeutic challenges now arise?
There are bilateral MCA aneurysms. Which are approximately the same size. Mirror aneurysms in this configuration are seen occasionally. There is vasospasm of the right MCA M1 segment which is narrowed and irregular.
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What is important in a patient presenting with SAH and more than one aneurysm
It is important to establish which aneurysm has bled and therefore requires treatment. Sometimes more than one aneurysm may be treated in the same session. If a PCom and ACom aneurysm in a favourable configuration they could be coiled in the same session or clipped in the same operation on the same side.
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When is treatment of two aneurysms not possible
Not possible when either of the aneuryssm will require separate approach via right or left ICA or if neither can be coiled e.g. in bilateral MCA aneurysms clipping would need to happen via bilateral craniotomies.
106
What is an issue with a single surgical procedure to perform sequential bilateral MCAA clippings
Possible but more than doubles the risk to the patient of a single proceudre due to bilateral brain retraction. It is thus necessary to make a concerted effort to establish which aneurysm has bled.
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In the case of multiple aneurysms and SAH, how can one identify which aneurysm has bled?
Most commomn method is to review the pattern of SAH bleed on the presenting CT scan. The location of blood at presentation corresponds to aneurysm in around 80% of SAH.
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If there is no blood on CT, what is another option for identifying the site of aneurysmal bleed?
MRI can be used to look for asymmetric blood with greater sensitivity than CT There may also be signs of recent bleed at angiography e.g. Murphy's teat, localised vasospam around one more than another.
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Murphy's teat
Aneurysm morphology associated with a secondary bleb points to a higher rupture risk. This is more commonly seen at surgery but can be identified at angiography.
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What MRI sequence is most sensitive for recent SAH?
FLAIR (fluid attenuated inversion recovery)
111
Describe the image shown
Axial MRI flair sequence showing high signal on the right around the site of MCAA suggesting this is the aneurysm responsible for the bleed.
112
A 59-year-old man experienced a sudden-onset right-sided headache whilst walking in the street. He vomited and was unable to move his left side. He was brought by ambulance to the emergency department where his GCS was 8/15 (E1, V1, M6) and his pupils were equal and reactive. His blood pressure was 210/105mmHg. A CT scan was performed, and is shown Describe the appearances on the CT scan and features A–D.
There is a large high density lesion in the region of the thalamus representing acute harmorrhage The blood extends into the third ventricle, the frontal and occiptal horns of the lateral venticles. The frontal horns are dilated, indicating hydrocephalus
113
A 59-year-old man experienced a sudden-onset right-sided headache whilst walking in the street. He vomited and was unable to move his left side. He was brought by ambulance to the emergency department where his GCS was 8/15 (E1, V1, M6) and his pupils were equal and reactive. His blood pressure was 210/105mmHg. A CT scan was performed, and is shown Why is the patient hemiplegic?
The hemiplegia is due to the invovlement of the internal capsule, which lies adjacent to the thalamus and basal ganglia
114
A 59-year-old man experienced a sudden-onset right-sided headache whilst walking in the street. He vomited and was unable to move his left side. He was brought by ambulance to the emergency department where his GCS was 8/15 (E1, V1, M6) and his pupils were equal and reactive. His blood pressure was 210/105mmHg. A CT scan was performed, and is shown What is the diagnosis and what could be the cause
The pateint has suffered a spontaneous intracerebral haemorrhage. The DDx includes hypertensive haemorrhage, bleeding from underlying lesion suvch as AVM or tumour or coagulopathy. Hypertensive haemorrahge is most frequently seen in this location in a patient of this age.
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In which areas of the brain do hypertensive haemorrhages occur most often and why?
The most common location for spontaneous ICH is the BG \> cerebrum (lobar haemorrhage)\> cerebellum. These areas are susceptible because they are supplied by small arteries that directly branch off major arteries e.g. the lenticulostriate arteries supplying the basal ganglia and the thalamoperforating arteries supplying the thalamus. The walls of these susceptible arteries have been found to contain fat cells and fibrin-like material, a process termed lipohyalinosis and they develop microaneurysms (Charcot-Bouchard)
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Charcot-Bouchard aneurysms
Charcot–Bouchard aneurysms (also known as miliaryaneurysms or microaneurysms) are aneurysms of the brain vasculature which occur in small blood vessels (less than 300 micrometre diameter). Develop as a consequence of lipohyalinosis
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A 59-year-old man experienced a sudden-onset right-sided headache whilst walking in the street. He vomited and was unable to move his left side. He was brought by ambulance to the emergency department where his GCS was 8/15 (E1, V1, M6) and his pupils were equal and reactive. His blood pressure was 210/105mmHg. A CT scan was performed, and is shown What is the management of this patient?
Patients with spontaneous subcortical haemorrahge should be admitted to a stroke unit and receive IV fluids, DVT prophlyaxis and NGT as required. Surgery for spontaenous ICH is contraversial but is generally not recommended when the haemorrhage is subcortical and the deficit from the haemtoma is unlikely to impove. Treatment of the hydrocephalus may lead to a neurological improvment.
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What are the diversionary options for the treatment of hydrocephalus
LP Lumbar drain EVD
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A 59-year-old man experienced a sudden-onset right-sided headache whilst walking in the street. He vomited and was unable to move his left side. He was brought by ambulance to the emergency department where his GCS was 8/15 (E1, V1, M6) and his pupils were equal and reactive. His blood pressure was 210/105mmHg. A CT scan was performed, and is shown in F Options for treating hydrocephalus in this patient.
This patient has haemorrahge into the ventricles and performing an LP/drain in this situation carries the risk of coning. He underwent placement of an EVD
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Patient with ICH and intraventricular blood who developed hydrocephalus and underwent EVD insertion Five days after placement of the drain you are contacted by a nurse who is worried that the drain may be blocked. The patient has improved clinically since admission and his GCS is 14/15 (E4, V4, M6). What should be done now?
A blocked EVD can lead to an acutely raised ICP and is a potential emergency. Urgent assessment of the patient and the EVD apparatus is required. If the CSF swings in the drain when it is lowered obstruction is unlikely and the non-drainage is probably due to the EVD being set higher than CSF pressure. If the CSF does not swing, the drain is likely obstructed.
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Patient with ICH and intraventricular blood who developed hydrocephalus and underwent EVD insertion Five days after placement of the drain you are contacted by a nurse who is worried that the drain may be blocked. The patient has improved clinically since admission and his GCS is 14/15 (E4, V4, M6). The drain is flushed with saline but remains blocked and is removed. Does it need to be replaced?
This depends on whether ventricular drainage is still required and will be informed by a CTH to assess ventricular size
122
Patient with ICH and intraventricular blood who developed hydrocephalus and underwent EVD insertion Five days after placement of the drain you are contacted by a nurse who is worried that the drain may be blocked. The patient has improved clinically since admission and his GCS is 14/15 (E4, V4, M6). The EVD remains blocked despite flush and is removed. Repeat CTH is performed. Does this patient need another EVD, what other neurosurgical input is required?
The ventricles have decompressed and has clinically improved. Another EVD is not necessary. The patient requires ongoing stroke rehabilitation and an interval CT to check for recurrence of hydrocephalus and haemorrhage evolution
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CTH for a 59 y/o patient with acute onset left hemiparesis. What neurosurgical input is required?
This is a superficial lobar haemorrhage. There is no associated intraventricular blood or hydrocephalus. There may be an unproven benefit in these cases to relieve local mass effect and improve associated deficit. If the patient is otherwise medically well, direct evacuation of the haematoma would often be appropriate. Evacuation of the haematoma depends on whether the clot is thought to have caused the deficit by direct damage to eloquent brain or by local mass effect. In the latter situation, surgery is likely to have more benefit
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How would you manage a 69-year-old man with a cerebellar haematoma as shown ?
Cerebellar haematomas are more often treated surgically than supratentorial haematomas because the local mass effect can cause distortion of the fourth ventricle and obstructive hydrocephalus, the prevention of which results in a much better outcome. Many people will rehabilitate better from a bleed in the cerebellum rather than eloquent brain. This patient has early hydrocephlus and the surgical options are to treat the hydrocephalus only with an EVD, to evacuate the clot and anticipate the hydrocephalus will settle, or to evacute the clot and place an EVD at the same time with gradual wean over the next few days. Evacuation of clot would be preferred in this case as there is radiological evidence of brainstem compression which would not be relieved by EVD placement.
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STICH trial
Showed no significant difference in outcome in conservative vs surgical management of spontaneous intracerebral haematomas in which the clinician was unsure as to management
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What factors contribute to the risk of coning in the context of lumbar puncture
Mass lesions or obstructive hydrocephalus
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What should be done if a patient's conscious level deteriorates during LP?
Reintroduce CSF or saline to the subarachnoid space
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Placement of EVD
It involves placing a catheter within a ventricular cavity, most often the frontal horn of the lateral ventricle on the right side to minimise risk to the language area which is externalised through the skin and connected to a drainge device.
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How to level an EVD
The zero level of the manometer is placed at the level of the foramen Monro (external auditory meatus).
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How can the EVD be adjusted to set the ICP
The height of the manometer can be used. CSF will drain when intracranial pressure exceeds that level. At intracranial pressures less than this, CSF will swing in the tubing without draining ICP. A port is provided for sampling and antibiotic administration
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What are the indications for EVDs
Treatment of hydrocephalus: provides controlled, continuous drainge of CSF Treatment of ventriculitis: allows intrathecal Abx administration Continuous measurement of ICP
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Intraoperative complications of EVDs
Bleeding Malposition of drain Rarely, stroke (through drain malposition)
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Post-operative complications of EVD
Infection (skin, ventriculitis) CSF leak Blockage of drain Seizures
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What are the common problems with EVDs
Infection Blockage CSF leak
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Mx of EVD infection
Most frequent complication: leads to ventriculitis. The catheter should be replaced and intrathecal and IV Abx commenced
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Mx of EVD blockage
Check patency by lowering drain, if CSF swings, drain is patent. Check apparatus for disconnection or leaks Check tubing for debris Consider CT to check position of drain Consider aspiration Consider flushing drain with saline If you can flush but not aspirate from a drain that is not draining, the drain may be left in situ if it is being used for administration of Abx, otherwise it should be removed. If you cannot flush or aspirate from the drain which is not draining, it should be removed. Any manipulation of the EVD apparatus should be performed under sterile conditions
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Mx of CSF leak from EVD
Occurs where the drain exits scalp. Check drain length to see whether it has been displaced. Place a suture to tighten the space between the drain and scalp or lower drain level to drain more CSF through drain. A CSF leak must not be left to continue as it will result in ventriculitis
138
A 54-year-old man is referred from a local hospital. He has been admitted there following a sudden collapse. He has been persistently confused since the event with a severe headache. On examination he has a marked (2/5) weakness of his left arm; the leg is also weak but slightly less so. His GCS is 12/15 (E3, V3, M6) and his pupils are equal and reactive. His blood pressure is 130/80mmHg. The patient undergoes a CT scan (Fig. 22.1). What are the findings, what are the possible underlying diagnoses and how should he be managed?
There is a large right temporo-occipital intracerebral haematoma which has ruptured into the ventricles. There is moderate hydrocephalus. This is not a typical location for hypertensive haemorrahge. He is relatively young and is BP is not elevated. An underlying malformation is possible, most commonly an AVM. Haemorrhage from a tumour or cavernoma is possible but unlikely as typically these are more confined. The haemorrhage is parenchymal without any blood in the sylvian fissure so ruptured aneursym is unlikely. Early management is supportive. He is likely to need an EVD given the degree of hydrocephalus, intraventricular blood and neurological impairment. Surgery for the haematoma can be conisdered but the underlying cause should ideally be identified first so that intraoperative problems can be anticpated e.g. haemorrhage from an AVM
139
A 54-year-old man is referred from a local hospital. He has been admitted there following a sudden collapse. He has been persistently confused since the event with a severe headache. On examination he has a marked (2/5) weakness of his left arm; the leg is also weak but slightly less so. His GCS is 12/15 (E3, V3, M6) and his pupils are equal and reactive. His blood pressure is 130/80mmHg. CT scan is shown. 2. What vascular imaging should be offered, and why?
Many centres employ CTA for patients with SAH to look for intracranial aneurysms. if this patient has vascular pathology it is more likely to be an AVM\> Catheter angiography is preferred for AVM as it offers dynamic information during contrast injection and allows better visualisation of the feeding arteries supplying the AVM nidus as well as showing which veins drain the AVM. However, it is invasive and time-consuming to perform if the patient requires emergency surgery. In this case, a CTA should show abnormal vasculature prior to emergency surgery though it may not be sufficient for definitive elective treatment.
140
A 54-year-old man is referred from a local hospital. He has been admitted there following a sudden collapse. He has been persistently confused since the event with a severe headache. On examination he has a marked (2/5) weakness of his left arm; the leg is also weak but slightly less so. His GCS is 12/15 (E3, V3, M6) and his pupils are equal and reactive. His blood pressure is 130/80mmHg. He undergoes a CTA immediately and catheter angiogram 2 days later, which are shown What images are shown?
The images are an axial maximal intensity projection of the CTA An AP and lateral projection of the right ICA and an AP of the left vertebral artery angiogram
141
A 54-year-old man is referred from a local hospital. He has been admitted there following a sudden collapse. He has been persistently confused since the event with a severe headache. On examination he has a marked (2/5) weakness of his left arm; the leg is also weak but slightly less so. His GCS is 12/15 (E3, V3, M6) and his pupils are equal and reactive. His blood pressure is 130/80mmHg. He undergoes a CTA immediately and catheter angiogram 2 days later, which are shown Identify the features labelled 1-6
1- haematoma with some abnormal blood vessels posterolateral to the haematoma bed (2). There appears to be some supply to them from the right PCA. The carotid angiogram shows the abnormal tangle of vessels coming through a fetal PComm (4) which partly feeds the PCA (5). The vertebral angiogram also shows supply from the PCA and in addition during the arterial phase as shown there is filling from the veins draining the AVM before the normal cerebral venous phase. Early venous filling is the hallmark of arteriovenous shunting. Overall the nidus is around 2.5cm in diameter
142
A 54-year-old man is referred from a local hospital. He has been admitted there following a sudden collapse. He has been persistently confused since the event with a severe headache. On examination he has a marked (2/5) weakness of his left arm; the leg is also weak but slightly less so. His GCS is 12/15 (E3, V3, M6) and his pupils are equal and reactive. His blood pressure is 130/80mmHg. He undergoes a CTA immediately and catheter angiogram 2 days later, which are shown What is the abnormality and what are its salient features?
The arterial supply and venous drainage of the AVM are the most important features along with the overall size. If endovascular therapy is to be attempted, either prior to surgical resection or radiosurgery, the vessels supplying the AVM must be wide enough to allow catheter access. Similarly, if these vessels also supply eloquent brain close to the AVM nidus, achieving safe catheter position for embolisation will be more difficult and the risk of embolisation causing stroke higher.
143
Surgical planning for AVM
Requires knowledge of the arterial supply so that appropriate vessels can be ligated in turn before nidus excision
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What is the importance of establishing venous drainage of AVM prior to surgical management?
Venous drainage must be established and ligated before nidus excision otherwise intranidal pressures will rise and this may cause severe intraoperative harmorrahge
145
What is the importance of establishing AVM nidus size
AVM \<3cm in diameter may be treated with stereotactic radiosurgery.
146
What is the delay following treatment of AVM with stereotactic radiosurgery
There is usually a lag between 2 and 5y before radiosurgery results in obliteration, it is a treatment with low morbidity and therefore is preferred for smaller AVMs in eloquent brain areas
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What are the treatment options in AVM
Conservative Embolisation alone with curative intent Surgery alone Radiosurgery alone Embolisation followed by surgery or radiosurgery
148
Features of embolisation for AVM
Embolisation alone is not usually curative and should be performed for larger AVMs prior to surgery. It may be tried with curative intent in surgically inaccessible lesions. following failed radiosurgery or with palliative intent for large AVMs presenting with unusual features (e.g. steal phenomena or hydrocephalus)
149
What can be used to grade surgical risk for AVMs?
Spetzler-Martin scale
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What are the areas of scoring for the Spetzler-Martin scale
Eloquence of surrounding brain Presence of deep draining veins Size of nidus
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Spetzler Martin scale Eloquence of surrounding brain
Eloquent (1) Non-eloquent (0)
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Spetzler-Martin scale Presence of deep draining veins
Present 1 Absent 0
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Spetzler Martin scale Nidus size
\<3cm, 1 3-6cm 2 \>6cm 3
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What is the clinical significance of the Spetzler-Martin scale
Scores range from 1-5. For grade 1 AVMs, the surgical morbidity and mortality should be very low and surgery is the treatment of choice. For larger AVMs in non-eloquent brain, embolisation should be performed prior to surgery Smaller, eloquent AVMs should be managed with radiosurgery, possibly in combination with prior embolisation. High grade (4/5) are considered inoperable and should be treated with embolisation to reduce the size of the nidus and then be re-evaluated
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Risk of second haemorrhage for AVM
Far lower than for aneursyms, 5-17% per year compared with 2% per day and therefore there is not the same mandate for urgent excision. If the patient is sufficently well there is a strong argument for early surgery in AVM.
156
A 60-year-old man presented with a 2-month history of progressive unsteadiness. He reported having a painful sensation over the previous 18 months which began in the feet and gradually ascended in the legs. Intermittently, he also found it difficult to pass urine. His medical history was unremarkable and he was not on regular medication. On examination, he was alert and orientated. In the lower limbs, the tone was increased, power was normal, and reflexes were brisk. Proprioception was impaired bilaterally in the toes and plantars were upgoing bilaterally. Romberg’s test was negative and there were no cerebellar signs. A sensory level was identified at the level of T3. The upper limbs were normal. Where is the lesion likely to be?
The signs point to a lesion in the upper thoracic spinal cord. This is supported by the UMN signs in the lower limbs, T3 sensory level and extensor plantars. Impaired proprioception in this context suggests dorsal column involvement
157
How do spinal cord lesions lead to problems with micturition?
It can interfere with the central micturition pathway which runs in the spinal cord.
158
A 60-year-old man presented with a 2-month history of progressive unsteadiness. He reported having a painful sensation over the previous 18 months which began in the feet and gradually ascended in the legs. Intermittently, he also found it difficult to pass urine. His medical history was unremarkable and he was not on regular medication. On examination, he was alert and orientated. In the lower limbs, the tone was increased, power was normal, and reflexes were brisk. Proprioception was impaired bilaterally in the toes and plantars were upgoing bilaterally. Romberg’s test was negative and there were no cerebellar signs. A sensory level was identified at the level of T3. The upper limbs were normal. How should this patient be managed?
This gentleman requires an urgent MRI scan of the spine. He also requires a pre and post-void bladder scan. If a residual volume is found, urologoy opinion should be sought
159
A 60-year-old man presented with a 2-month history of progressive unsteadiness. He reported having a painful sensation over the previous 18 months which began in the feet and gradually ascended in the legs. Intermittently, he also found it difficult to pass urine. His medical history was unremarkable and he was not on regular medication. On examination, he was alert and orientated. In the lower limbs, the tone was increased, power was normal, and reflexes were brisk. Proprioception was impaired bilaterally in the toes and plantars were upgoing bilaterally. Romberg’s test was negative and there were no cerebellar signs. A sensory level was identified at the level of T3. The upper limbs were normal. He undergoes an MRI which is shown Describe the findings A to C. What is the diagnosis What further investigations are mandated?
There is an area of diffuse high signal in the spinal cord extending from T3/4 to T12 (A) Prominent vessels are present around the cord between these levels indicated by small areas of hypointensity or flow voids on the cord surface (B). These appearances are highly suggestive of a spinal vascular malformation. A mild disc bulge is also present (C) which is not compressing the spinal cord and therefore unrelated to the presenting symptoms
160
Describe the vascular supply of the spinal cord
The spinal cord is supplied by an arterial anastomotic network consisting of the anterior spinal artery, paired posterior spinal arteries and anterior and posterior segmental arteries arising from the vertebral, posterior intercostal, lumbar or sacral arteries depending on the SC level which enter the spinal canal through the intervertebral foramina. Segmental arteries supply the spinal nerve roots and may extend intradurally to anastomose with the anterior or posterior spinal arteries. The spinal veins have a similar configuration to the arteries. There are usually 3 anterior and 3 posterior spinal veins that lie on the surface of the SC and drain into the epidural venous plexus. This drains into segmental veins but also communicates with the intracranial venous sinuses through the foramen magnum
161
How are spinal vascular malformations classified?
Kim-Speltzer classficiation
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Type 1 spinal vascular malformation
SCDAVF Dural AVF in which a segmental artery forms a fistula with a draining vein at the dural sleeve of a nerve root
163
Type 2 spinal vascular malformation
SCAVM (Glomus) Lesions consist of a compact intramedullary nidus
164
Type 3 spinal vascular malformation
Juvenile SCAVM Juvenile lesions are large intramedullary lesions which may extend extradurally or extraspinally.
165
Type 4 spinal vascular malformations
SCAVF Intradural, extramedullary AV fistulas with a direct connection between the vascular supply of the spinal cord and a vein
166
What is the most common spinal vascular malformation
Type 1.
167
How can spinal dural fistulas cause myelopathy? Why would this cause symptoms that develop in an ascending fashion?
In Type 1 spinal AVMs, AV shunting leads to chronic venous hypertension in the intradural venous system. This leads to slower flow in the arterial system, impaired oxygenation and subsequent ischaemic myelopathy. Spinal cord oedema begins in the most dependent part of the cord, hence symptoms are usually of an ascending nature. In extradural AVMs, myelopathy may occur due to compression of the cord due to engorged extradural veins.
168
A 60-year-old man presented with a 2-month history of progressive unsteadiness. He reported having a painful sensation over the previous 18 months which began in the feet and gradually ascended in the legs. Intermittently, he also found it difficult to pass urine. His medical history was unremarkable and he was not on regular medication. On examination, he was alert and orientated. In the lower limbs, the tone was increased, power was normal, and reflexes were brisk. Proprioception was impaired bilaterally in the toes and plantars were upgoing bilaterally. Romberg’s test was negative and there were no cerebellar signs. A sensory level was identified at the level of T3. The upper limbs were normal. He is found to have a type 1 spinal AV malformation What is the management of this case?
The patient has progressive symptoms and therefore should be offered treatment to obliterate the fistula. The options are surgical divison or endovascular embolisation
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Surgical divison of spinal AV fistula
Offers the highest rate of sucess though with associated risks of open surgery
170
Endovascular management of spinal AV malformation
The endovascular option is associated with an appreciable recurrence rate, approximately 50%
171
A 35-year-old man presents with a sudden onset of severe headache that occurred whilst gardening. He is a previously healthy non-smoker. Of note, when aged 26 he suffered a single generalized seizure that was not investigated. In the emergency department he is alert and orientated with no photophobia or neck stiffness, and his headache is settling by the time he is reviewed after 4 hours. He has no discernible neurological deficit. What is the DDx?
DDx includes vascular events such as SAH Other types of intracranial haemorrhage should be considered though they would more frequently be associated with neurological deficits. Non haemorrhagic causes such as migraine and cluster headache should be considered though typically patients will have a prior history
172
A 35-year-old man presents with a sudden onset of severe headache that occurred whilst gardening. He is a previously healthy non-smoker. Of note, when aged 26 he suffered a single generalized seizure that was not investigated. In the emergency department, he is alert and orientated with no photophobia or neck stiffness, and his headache is settling by the time he is reviewed after 4 hours. He has no discernible neurological deficit. He undergoes CTH. What does it show?
There is a well-circumscribed subcortical hyperdensity in the right parietal region with an appreciable amount of surrounding oedema. This is an acute haemorrhage The location and age of the patient mandate a search for an underlying abnormality that may have bled such as a tumour or vascular malformation. If no structural lesion is found the patient should be investigated for medical causes such as vasculitis or amyloid angiopathy
173
A 35-year-old man presents with a sudden onset of severe headache that occurred whilst gardening. He is a previously healthy non-smoker. Of note, when aged 26 he suffered a single generalized seizure that was not investigated. In the emergency department he is alert and orientated with no photophobia or neck stiffness, and his headache is settling by the time he is reviewed after 4 hours. He has no discernible neurological deficit. He undergoes CTH. What are the management options?
The management should initialy be conservative given the good neurological condition. If he deteriorates repeat imaging should be performed to look for further haemorrhage. In planning further Ix the underlying cause should be considered. The bleed has none of the features of an aneurysmal haemorrhage and further investigation is probably not necessary. MRI scanning should be delayed for 6/52 to allow the haematoma to involute to increase diagnostic certainty. Angiography may be required depending on MRI findings
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A 35-year-old man presents with a sudden onset of severe headache that occurred whilst gardening. He is a previously healthy non-smoker. Of note, when aged 26 he suffered a single generalized seizure that was not investigated. In the emergency department he is alert and orientated with no photophobia or neck stiffness, and his headache is settling by the time he is reviewed after 4 hours. He has no discernible neurological deficit. He undergoes CTH. He goes home with OP MRI arranged for 6/52 time. What would you advise the patient.
General advice about what to do if there were recurrence of symptoms and the need to return to hospital. He must not drive due to the presence of supratentorial haemorrhage of unknown aetiology and the associated risks of seizures. For the same reason he should be counselled about swimming alone and working in dangerous situations
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A 35-year-old man presents with a sudden onset of severe headache that occurred whilst gardening. He is a previously healthy non-smoker. Of note, when aged 26 he suffered a single generalized seizure that was not investigated. In the emergency department he is alert and orientated with no photophobia or neck stiffness, and his headache is settling by the time he is reviewed after 4 hours. He has no discernible neurological deficit. His headache settles and he goes home. An MRI scan is perofmed at 6/52 as planned and is shown. What does it show and what is the diagnosis? Should he have an angiogram?
The coronal T1, axial T2 and axial T1 post contrast scans are shown. The abnormality and an associated fluid-filled cavity within it are seen. The mass has high signal elements on T1 and low signal elements with a black rim on T2. It does not enhance. These are charactersitic findings of a cavernoma however a metastasis is still possible. An angiogram is not reuqired, it would probably be normal although a late venous blush may be seen reflecting the venous nature of the vascular channels in the cavernoma. The near-normal angiographic appearances of cavernomas has led them to being described as angiographically occult vascular malformations
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What is the characteristics MRI appearance of cavernoma
High signal elements on T1, low signal on T2. No appreciable enhancement. May have a black rim which represents haemosiderin deposts after acute haemorrhage
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What is the natural history of cavernomas?
Cavernomas are characterised by recurrent haemorrhages that are typically small as they are under venous pressure. A cavernoma in the parietal lobe is unlikely to be life-threatening. Surgery is typically curative and depending on the location may carry low morbidity. The principle risks of surgery would be epilepsy and focal neurological deficits. The risks of not treating a patient such as the one in the case discussed is low. Surgery may not be offered unless patients have difficulty with the uncertainty of conservative management.
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What is the annual risk of haemorrhage from cavernoma?
0.5-2%
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Non-dominant parietal lobe syndrome
Problems with spatial perception, classically getting lost in an otherwsie familiar location. Dressing apraxia
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What is the role for radiosurgery for cavernomas?
Has been used extensively with safety and good long term results for intracranial AVMs. It has also been used for cavernomas with equivocal results. It appears to be safe and thus may be given if there is no alternative and conservative management is not acceptable. It is more appropriate for surgically inaccessible lesions such as those in the thalamus or brainstem.
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How would you advise a patient who presented with diplopia and was found to have a single haemorrhage from a cavernoma located in the brainstem as shown
The patient should be told of the diagnosis but reassured that the risks of recurrent haemorrhage are statistically low but that this may be more clinically apparent in eloquent areas of the brain such as the brainstem. A gradual recovery is to be expected and rehabilitation with ophthalmological follow up if the diplopia doesn't resolve. He may be disqualified from driving because of his diplopia. Surgery would only be considered for brainstem cavernomas with recurrent bleeds, progressive deficits with a lesion that is surgically accessible. Radiosurgery may be the only option though outcomes are equivocal.
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A 55-year-old man arrived in the emergency department having been found collapsed in his kitchen 6 hours previously. He was last seen well by his wife an hour before he was found. On arrival in the emergency department, he was alert and eye-opening spontaneously, and obeying commands with his left hand (he was unable to move his right side). He was attempting to speak but was unable to do so. His pulse rate was 126bpm and the rhythm was atrial fibrillation. His blood pressure was 203/110mmHg What is the patient's GCS
His GCS is E4, VD, M6= 10 He is unable to speak, presumably due to damage to the language areas in the lest hemisphere. His verbal score is therefore recorded as D (dysphasic)
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What is the verbal score on the GCS when a patient is intubated?
T
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A 55-year-old man arrived in the emergency department having been found collapsed in his kitchen 6 hours previously. He was last seen well by his wife an hour before he was found. On arrival in the emergency department, he was alert and eye-opening spontaneously, and obeying commands with his left hand (he was unable to move his right side). He was attempting to speak but was unable to do so. His pulse rate was 126bpm and the rhythm was atrial fibrillation. His blood pressure was 203/110mmHg What type of dysphasia does this patient have?
This patient has an expressive dysphasia as he is obeying commands, indicating that his comprehension is intact
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A 55-year-old man arrived in the emergency department having been found collapsed in his kitchen 6 hours previously. He was last seen well by his wife an hour before he was found. On arrival in the emergency department, he was alert and eye-opening spontaneously, and obeying commands with his left hand (he was unable to move his right side). He was attempting to speak but was unable to do so. His pulse rate was 126bpm and the rhythm was atrial fibrillation. His blood pressure was 203/110mmHg CT scan is performed. Describe the lesion.
There is a large area of low attenuation in the left frontal, temporal and parietal regions and in the posterior basal ganglia. This is an acute infarct and it involves the entire left MCA. There is also some early haemorrhagic transformation as evidenced by high density in the left putamen. The caudate head is spared as it is supplied by the ACA perforators. There is effacement of the frontal horn of the left lateral ventricle with midline shift. There is also contralateral compartmental hydrocephalus of the trigone of the right lateral ventricle
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A 55-year-old man arrived in the emergency department having been found collapsed in his kitchen 6 hours previously. He was last seen well by his wife an hour before he was found. On arrival in the emergency department, he was alert and eye-opening spontaneously and obeying commands with his left hand (he was unable to move his right side). He was attempting to speak but was unable to do so. His pulse rate was 126bpm and the rhythm was atrial fibrillation. His blood pressure was 203/110mmHg What is the medical management of this case?
Thrombolysis would be considered for acute ACA but this is not appropriate as the presentation is too late and there is evidence of haemorrhage. The patient should receive aspirin, IVF, thromboprophylaxis with IPB, swallowing assessment and NG tube if necessary for feeding and medication. A) Management of BP B) Management of AF with FVR C) Ix to establish the underlying aetiology of the stroke
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Management of BP in stroke
In general hypertension in the immediate period after stroke is best left alone. If antihypertensives are used an IV infusion that can be stopped readily should be used
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Ix after stroke
Carotid doppler Echo for thrombi, valve disease, septal defets Routine bloods including CV risk profile
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A 55-year-old man arrived in the emergency department having been found collapsed in his kitchen 6 hours previously. He was last seen well by his wife an hour before he was found. On arrival in the emergency department, he was alert and eye-opening spontaneously, and obeying commands with his left hand (he was unable to move his right side). He was attempting to speak but was unable to do so. His pulse rate was 126bpm and the rhythm was atrial fibrillation. His blood pressure was 203/110mmHg Is this patient a candidate for decompressive craniectomy?
There are three randomised trials, DESTINY, DECIMAL, HAMLET comparing decompressive hemicraniectomy with medical management for malignant MCA infarction. None of the studies showed a difference in primary outcome though a meta-analysis of the three studies appears to show that surgery reduces mortality in patients under the age of 60 who undergo surgery withn 48h. Many although not all patients who are salvaged with surgery are left with a signfiicant disability
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What factors influence the decision to operate in malignant MCA infarct
Made on an individual basis taking into account the patient's neurological status, previous level of functioning and comorbidities
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A 55-year-old man arrived in the emergency department having been found collapsed in his kitchen 6 hours previously. He was last seen well by his wife an hour before he was found. On arrival in the emergency department, he was alert and eye-opening spontaneously and obeying commands with his left hand (he was unable to move his right side). He was attempting to speak but was unable to do so. His pulse rate was 126bpm and the rhythm was atrial fibrillation. His blood pressure was 203/110mmHg This patient underwent decompressive craniectomy which is shown. Describe the scan
Note the brain herniating through the craniectomy defect and the resolution of the midline shift. The outcome without surgery would have been transtentorial herniation. After surgery, this patient remained hemiplegic and aphasic and was transferred to a neuro-rehab centre. If he regians independence a cranioplasty will be required at a future data, the bone window CT scan shown was used to plan the prosthesis
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A 68-year-old woman presented with a sudden onset of left arm weakness whilst eating breakfast such that she dropped her fork and was unable to pick it up. This lasted for around 30 minutes, after which there was a gradual recovery to normal. She attended the emergency department where a CT scan was performed. The contrast enhanced scan is shown in Fig. 26.1. Her medical history includes coronary heart disease, diabetes, hypertension, and multiple strokes. What does the scan show and does it explain her symptoms?
The scan shows a circular hyperdense area adjacent to the right MCA which is likely to be an aneurysm. Note that the density is the same as the adjacent blood vessels. There is no subarachnoid blood suggesting that this is an incidental finding. There are small low-density areas in the left side of the pons which may be due to small vessel disease. It was felt her symptoms were more likely explained by a TIA
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A 68-year-old woman presented with a sudden onset of left arm weakness whilst eating breakfast such that she dropped her fork and was unable to pick it up. This lasted for around 30 minutes, after which there was a gradual recovery to normal. She attended the emergency department where a CT scan was performed. The contrast-enhanced scan is shown in Fig. 26.1. Her medical history includes coronary heart disease, diabetes, hypertension, and multiple strokes An incidental right MCAA is found, her symptoms are attributed to a TIA. What is the initial step in the management of this case? Does the patient need to be admitted to hospital
The initial management is to investigate the TIA in a conventional manner with echo, carotid doppler and risk factor control The subsequent risk of aneurysm rupture should be weighed against the risks of the procedure to secure the aneurysm. The rupture risk of an aneurysm of this size is about 0.5-1% per year. The patient does not have to be admitted to hospital
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Why are unruptured intracranial aneurysms increasing in incidence?
More people are undergoing high resolution brain imaging for smyptoms in the past that would not have warranted imaging of sufficient quality to show an aneurysm. Increased education of the relatives of patients with SAH is resulting in more screening investigations for first-degree relatives
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What is the most common visual disturbance in the symptomatic presentation of unruptured aneurysms
Visual disturbance, typically a CN3 palsy due to PComm or SCAA or reduced acuity in one eye due to optic nerve compression by an ophthalmic artery or terminal carotid aneuryms.
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Presentation of unruptured giant aneurysms (\>25mm)
Can occasionally present with cortical deficits due to mass effect. Large aneurysms are usually lined with thrombus and if there is turbulent flow within the aneurysm this thrombus may act as a source of emboli. Aneurysms may thus present with TIAs in the downstream territory
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What is the principle indication for surgical management of unruptured aneurysms?
Treated specifically to prevent rupture. Large aneurysms are difficult to clip or coil and may require complex vascular surgical procedures including bypass.
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What are the factors that influence decision-making around treatment of an unruptured intracranial aneurysm?
What is the life expectancy of the patient? What is the annual risk of rupture? What are the consequences of aneurysmal rupture likely to be e.g. cavernous carotid aneurysms may cause a carotid-cavernous fistula which is a more benign problem than SAH. How can the aneurysms be treated, is it suitable for coiling, what are the risks associated for surgery if it is suitable for clipping?
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What was used to establish the risk of rupture of unruptured aneurysms?
The International Study of Unruptured Intracranial Aneurysms
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Classifications of aneurysms in ISUIA
Anterior- ICA, ACA, AComm, MCA or Posterior PCom, basilar, PCA
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Of what should patients who undergo aneurysmal repair be advised?
Risk of recurrence is increased fourfold if they continue to smoke
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Which type of aneurysm is more likely to rupture according to ISUIA, anterior or posterior?
Posterior
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A 43-year-old woman is admitted with a sudden severe headache in good neurological condition. She has marked photophobia and is vomiting. Her CT scan shows subarachnoid blood and angiograms confirm a right PCom aneurysm. The patient undergoes coiling of the aneurysm as in view of the neck it is considered likely to provide a good angiographic result. The angiograms before and after coiling are shown in Fig. 27.1. She makes a good recovery which continues when she is seen in outpatients 6 weeks later. How would you follow her up and when?
Follow up is not to detect imminent rupture but rather to detect recurrence of the aneurysm neck which might over time result in an unstable aneurysm with a risk of re-rupture. CTA is the modality of choice for diagnosis of ruptured aneurysm initially but there will be too much artefact from the coils to make it of any value in the surveillance of a coiled aneurysm. MR angiography or catheter angiography can be used instead.
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Risk of catheter angiography
Arterial puncture Stroke
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When should catheter angiography be used for aneurysm surveillance after coiling?
When MRA is unclear
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Timing of follow up imaging after aneurysm coiling?
An early post-procedure MRA may be done to offer baseline comparison for the next scan which may be done at 6/12 assuming the coiling is deemed satisfactory. If scans at 6/12 and 12/12 show stable appearances, the follow up interval is increased
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Screening for intracranial aneurysms
Should be offered to any individual with two first-degree relatives with aneurysmal SAH. Patients with associated disease e.g. ADPKD may be offered a screening CTA or MRA. There are emerging groups of patients with lesser indications for screening angiography for example those with relatives with unruptured aneurysms. They may be offered screening but should be counselled that small aneurysms in difficult locations to access surgically may be left or monitored and that the act of screening may provoke more anxiety than assurances.
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A 43-year-old woman is admitted with a sudden severe headache in good neurological condition. She has marked photophobia and is vomiting. Her CT scan shows sub- arachnoid blood and angiograms confirm a right PCom aneurysm. The patient under- goes coiling of the aneurysm as in view of the neck it is considered likely to provide a good angiographic result. The angiograms before and after coiling are shown in Fig. 27.1. She makes a good recovery which continues when she is seen in outpatients 6 weeks later. The patient undergoes an MR angiogram which suggests a neck recurrence. This is evaluated with a catheter angiogram which is shown in Fig. 27.2. How does it compare to the previous angiogram at the end of the coiling?
There is appreciable recurrence of the neck of the aneursym due to compaction of coils into the dome
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A 43-year-old woman is admitted with a sudden severe headache in good neurological condition. She has marked photophobia and is vomiting. Her CT scan shows subarachnoid blood and angiograms confirm a right PCom aneurysm. The patient undergoes coiling of the aneurysm as in view of the neck it is considered likely to provide a good angiographic result. The angiograms before and after coiling are shown in Fig. 27.1. She makes a good recovery which continues when she is seen in outpatients 6 weeks later. The patient undergoes an MR angiogram which suggests a neck recurrence. This is evaluated with a catheter angiogram which is shown in Fig. 27.2. Given the patient’s age (45) and good recovery from the haemorrhage, the recurrence merits re-treatment. What are the options and which would you prefer?
The options are again endovascular or surgical management. The aim of treatment is now very different from the aim of the original coiling, the aim is now to protect the patient from rupture during the rest of her life. The aim before was to prevent early re-rupture which is most common during the first few weeks after the bleed. Open surgery for previously coiled aneurysm can be challenging as the coil ball may prevent a good closure of the aneurysm clip. It may be necessary to exclude the patent vessel temporarily, open the sac and remove the coils before clipping the aneurysm and then remove the temporary clips from the parent vessel. These manoeuvres increase the risk of surgical morbidity. Given that the patient has had aneurysm recurrence after endovascular intervention and the different aims of this secondary treatment, surgical management would be reasonable
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A 65-year-old woman presented to the neurosurgical clinic with a 2-week history of worsening left retro-orbital headache and double vision. On examination she had a left sixth nerve palsy. Seven years previously she had a similar presentation and was diagnosed to have a 15mm left carotico-ophthalmic aneurysm which was coiled at the time. On initial follow-up this had been stable with a small residual neck, but she had not been reviewed for the last 4 years. 1. What causes double vision?
Double vision can be monocular or binocular. Binocular diplopia is more frequently seen in neuroglocial disease and occurs when the two eyes do not move in synchrony. This may be due to dysfunction of the extra-ocular msucles themselves or their nerve supply, or the central pathways involved in conjugate eye movements. Monocular diplopia occurs due to problems within the eye iteself e.g. damage to the cornea, iris or lens
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A 65-year-old woman presented to the neurosurgical clinic with a 2-week history of worsening left retro-orbital headache and double vision. On examination, she had a left sixth nerve palsy. Seven years previously she had a similar presentation and was diagnosed to have a 15mm left carotico-ophthalmic aneurysm which was coiled at the time. On initial follow-up, this had been stable with a small residual neck, but she had not been reviewed for the last 4 years. 2. The patient has a left sixth nerve palsy on examination. Explain how she may have double vision on looking to both the left and right.
A left CN6 palsy leads to failure of abduction of the left eye and therefore diplopia on looking to the left. Diplopia on looking right may also occur in this situation because the balance of the globe is maintained by the tone of all the extra-ocular muscles. An alternative explanation is that she may also have a partial left CN4 palsy
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Why might a carotico-ophthalmic aneursym cause a CN6 palsy?
If a carotid aneurysm is wholly or partially within the cavernous sinus, as it expands it can compress structures in the lateral wall of the cavernous sinus, the nearest to it being the 6th nerve. If the aneurysm expands further it will compress more lateral structures- CN III, IV V1, 2
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What would the clinical manifestations of an expanding carotid aneurysm within the cavernous sinus?
Numbness on one side of the face though not in the jaw or lower teeth, complete ophthalmoplegia. You may expect the lateral rectus to be involved first due to its close association with the internal carotid in the medial wall of the cavernous sinus
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Complete ptosis Mid-position fixed eye Dilated pupil unresponsive to light
Complete ophthalmoplegia
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Painful sixth nerve palsy progressing to complete ophthalmoplegia is very suggestive of what?
Enlarging intracavernous carotid aneurysm.
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Retro-orbital headache, blurred vision in the affected eye, chemosis and proptosis along with the sign of an audible pulsatile bruit over the eye.
Carotid aneurysm rupture causing a carotico-cavernous fistula. If there is an intradural segment to the aneurysm, a rupture of this section would lead to SAH which is potentially life-threatening
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A 65-year-old woman presented to the neurosurgical clinic with a 2-week history of worsening left retro-orbital headache and double vision. On examination, she had a left sixth nerve palsy. Seven years previously she had a similar presentation and was diagnosed to have a 15mm left carotico-ophthalmic aneurysm which was coiled at the time. On initial follow-up, this had been stable with a small residual neck, but she had not been reviewed for the last 4 years. 4. The patient underwent an MRI scan of the brain (T2-weighted axial slice shown) and a cerebral angiogram (Fig. 28.1). Describe the important findings.
The MRI shows a left-sided 30mm mass located medial to the left temporal lobe and arising in the region of the carotid artery. The angiogram confirms this to be a cerebral aneurysm arising from the proximal intradural ICA. The posterior rim of the aneurysm does not fill with intra-arterial contrast and shows low signal on the MRI where the previously inserted coils were placed
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Patient with a 30mmm intradural internal carotid artery aneurysm. What is the prognosis?
This would be considered a giant aneurysm, with the prognosis being poor even if unruptured. The risk of rupture death or serious permanenet neurological deficit being \>50% within 1y. Giant aneurysms can be symptomatic if they rupture or they can cause ischaemic infarction by throwing off thrombotic emboli into their distal arterial territory.
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What are the options for treatment of giant carotocavernous aneurysm
Operative clipping can sometimes be undertaken but often has a higher risk of stroke and may have to be considered under cardiac bypass and hypothermic cerebral circulatory arrest. Coiling and stenting can sometimes be an option but still carry appreciable risks of stroke or death. Balloon occlusion of the feeding artery into a giant aneurysm can often be the best option provided that it is tolerated during a test occlusion without inducing a neurological deficit. This usually allows complete occlusion of the aneurysm with no risk of recurrence and a minimal physiological insult to the patient as the procedure is endovascular. If the cerebral collateral circulation is not enough to tolerate this and the patient develops a temporary deficit when performing a test occlusion, it is possible to perform surgical extracranial to intracranial bypass procedure to augment the cerebral blood flow to the affect distal circulation of the brain Patient can then subsequently undergo delayed balloon occlusion 1/12 later
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What is the procedure for EC-IC bypass?
Usually the superficial temporal artery or a segment of radial artery joint to the caroid artery in the neck can be anastomosed onto a branch of the MCA The CTA shows the presence of a superficial temporal artery branch transversing through a craniotomy defect and joining onto a vessel on the cerebral surface
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What are some additional indications for EC-IC procedures?
Can be used to treat chronic cerebral haemodynamic insufficiency as a result of ICA occlusion causing haemodynamic TIAs or progressive strokes in patients with proven low blood flows in the ischaemic territory. Such patients typically develop a stereotyped neurological deficit when their cerebral perfusion might be reduced fro example when dehydrated or experiencing a postural drop. Patients with high-grade carotid stenosis could have an endarterectomy or carotid stenting to help improve CBF if they are developing haemodynamic TIAs. Can also be considered for moyamoya disease
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Moyamoya disease
Rare, idiopathic progressive cerebrovascular disease seen in children or young adult patients. Initially causes ischaemic stroke but later develops an increased risk of intracerebral bleeds as new abnormal fragile perforator arteries enlarge and attempt to supply the ischaemic regions of the brain
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FLAIR sequence
Fluid attenuation inversion recovery Special inversion recovery sequence with a long inversion time. Removes signal from CSF from the resulting images. Brain tissue on FLAIR images therefore appears similar to T2 weighted images with grey matter brighter than white but CSF is dark instead of bright.