NEUROLOGY ANSWER PAPER

SATURDAY 28/11/2015

List 4 causes of neck stiffness

[ Hide Answer ]

College Answer

° Meningitis/encephalitis

° Subarachnoid hemorrhage

° Post fossa syndrome

° Tetanus

° Cervical spondylitis

° Neck abscess

° Wry neck / Torticollis

Discussion

To this predictable list, I could also add

dural sinus thrombosisepidural abscesscervical facet joint arthritis"whiplash" - musculoskeletal hyperextension injury

And many others. One can go right to town on this. Consider a cause for neck stiffness from any of the

major pathological categories, and I guarantee you will find one.

Observe:

Vascular:

Dural sinus thrombosisSubarachnoid hemorrhage

Infectious:

Epidural abscessNeck abscessMeningitis/encephalitisTetanus

Neoplastic:

C-spine vertebral metastasis or primary

Drug-related:

Home » CICM Fellowship Exam » Past Papers » 2009, Paper 1 SAQs

estion 24.5

Dystonic reactionWithdrawal

Idiopathic/inflammatory:

OsteoarthritisCervical spondylitisTorticollis

Autoimmune:

Rheumatoid arthritisAnkylosing spondylitis

Traumatic

WhiplashC-spine dislocation, subluxation or fractureProlonged neck hyperextension during surgery (eg. tracheostomy)

Endocrine:

Hypocalcemia

List 4 clinical signs which may be noticeable on examination of the head in a patient with cerebellar

disease.

[ Hide Answer ]

College AnswerNystagmusTitubationStaccato speechSkew deviation of the eyesImpairment of finger-nose test

Discussion

is question interrogates one's knowledge of the highly regarded Talley and O'Connor manual of physical

examination.

Talley and O'Connor visits the cerebellum twice, once in the chapter on the neurological examination of

the head, and once in the discussion of "Correlation of physical signs and neurological disease". Neither

time is there discussion of what specifically to look for in the patient's head. Its just not that specific.

Similarly, L.I.G Wortheley in the 3rd edition of CECIP (Clinical Examination of the Critically Ill Patient)

makes mention of the cerebellum, but does not actually go through it in quite such a fashion.

So, where does one go for a thorough summary of what one can expect from a cerebellum-damaged head?

It seems, nowhere.*

ankfully, from our medical school days, it seems about 84% of us can remember at least a few of the

cerebellar signs. But, in searching for the specific signs mentioned by the college, I came across something.

A website by the Coopers. ese seem to be a couple who have moved from Australia to Ohio. is, in a

deliciously unexplained twist, is completely irrelevant to the extravagant and all-encompassing mass of

neurological examination material which abounds on their site. I have taken the liberty of linking to some

of the documents they host.

Bob and Christina Cooper, I salute you.

* Several years aer writing this rant, I have discovered a venerable document from 1990, available forfree for all to read, which conveniently divides the cerebellar examination into body regions. isresource has subsequently given rise to a locally available summary of cerebellar physical signs andexamination technique. e obsolete rant still remains in situ for structural reasons. - A.(2015)

Home » CICM Fellowship Exam » Past Papers » 2011, Paper 2 SAQs

estion 26.1

References:

Schmahmann JD (2004). "Disorders of the cerebellum: ataxia, dysmetria of thought, and the cerebellar

cognitive affective syndrome". J Neuropsychiatry Clin Neurosci (3): 367–78

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered

from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where.

My own gibberish notes from medical school.

Walker, H. Kenneth, W. Dallas Hall, and J. Willis Hurst. "e Neurologic System." (1990). Specifically:Chapter 69, "e Cerebellum"

A 64-year-old male has been an in-patient in your Intensive Care Unit for one week following a

subarachnoid haemorrhage.

e following data were obtained from a CSF sample taken from the external ventricular drain:

Parameter Patient Value Normal Adult Range

Glucose 3.8 mmol/L 2.2 – 3.9

Protein 0.46 G/L 0.15 – 0.5

White Cell Count 20x106 /L* < 5

Red Cell Count 10 000x106 /L* < 5

Interpret these results.

[ Hide Answer ]

College Answer

e WCC is elevated but the WCC:RCC ratio is normal (1:500) and represents normal findings aer sub-

arachnoid haemorrhage but does not exclude infection.

Discussion

is is a faily straightforward data interpretation question. 10,000 / 20 = 500; which is the perfect ratio. is

CSF is not infected, it just has blood in it.

Of course, in order to make a more accurate analysis, it would be good to also know the serum WCC, so

that one may calculate the proper ratio.

A more detailed discussion of CSF analysis is available elsewhere.

Home » CICM Fellowship Exam » Past Papers » 2013, Paper 2 SAQs

estion 3.2

A 27 year old male with a prolonged ICU stay following a subarachnoid

haemorrhage has a CSF specimen taken from his external ventricular drain.

e CSF gram stain result is:

Red Blood Cells 1946 x 106/L (0-5 x 106/L)

Polymorphs 198 x 106/L (0-5 x 106/L)

Mononuclear cells 74 x 106/L

Gram stain: scant gram positive cocci.

a). What is your assessment of the CSF result and provide a reason ?

b). List two likely organisms commonly reported on the Gram stain in this seing.

c). List 2 therapies you may consider based on this report .

[ Hide Answer ]

College Answer

a). What is your assessment of the CSF result and provide a reason ?

Ventriculitis : due to raised WCC:RCC ratio and a positive gram stain

b). List two likely organisms commonly reported on the Gram stain in this seing.

Staphylococcus epidermidis

Staphylococcus aureus

c). List 2 therapies you may consider based on this report .

Removal of EVD / replacement

Vancomycin

Discussion

is patient has ventriculitis. e ratio of WCCs to RBCs is around 1:10, rather than 1:500-1500. erefore,

there is "CSF pleocytosis". e presence of monocytes is also much higher than would be expected purely

from the presence of the EVD.

e gram positive cocci found in this CSF sample are likely tourist organisms from the skin, which took a

ride into the brain on the back of the EVD. Likely, these are going to be either Staphylococcus aureus,Staphylococcus epidermidis or Streptococcus pyogenes.

Home » CICM Fellowship Exam » Past Papers » 2008, Paper 2 SAQs

estion 11.1

e two things one should immediately consider is

1) Get the infected EVD out

2) Start some antibiotics, which in the context of unknown sensitivities should consist of cephalosomething

and vancomycin.

e normal properties and contents of the CSF are discussed in detail elsewhere.

Meningitis is favoured with a chapter in Oh's Manual, and is also discussed elsewhere.

References:

Beer, R., P. Lackner, and B. Pfausler. "Nosocomial ventriculitis and meningitis in neurocritical care

patients." Journal of neurology 255.11 (2008): 1617-1624.

A patient presented with sudden onset of weakness involving his le upper and lower limb. On

examination, he was conscious, with a dilated non-reactive right pupil, normal power in the right upper

and lower limbs, and a le hemiparesis. What is the likely site of lesion? Outline your reasoning.

[ Hide Answer ]

College Answer

Right side of the midbrain. It is a crossed hemiplegia suggesting a brainstem stroke and the 3rd nerve

nucleus is located in the midbrain.

Discussion

is question interrogates one's knowledge of the highly regarded Talley and O'Connor manual of physical

examination.

Let us reason through this. A le hemiparesis suggests right sided cerebral pathology.

A right sided unreactive pupil suggests that the third nerve is somehow involved, and the nucleus for it is

in the midbrain. Ergo, the right midbrain has infarcted. e hemiparesis reflects damage to the right-sided

motor tracts above the level of the decussation (which is at the medulla).

References:

e Internet Stroke Centre has an excellent summary of stroke syndromes.

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered

from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired wherever good books are

sold or stolen.

Home » CICM Fellowship Exam » Past Papers » 2011, Paper 2 SAQs

estion 26.2

You are asked to admit a 76-year-old man with a past history of ischaemic heart disease and paroxysmal

atrial fibrillation who has just been intubated in Accident and Emergency aer collapsing from a brain stem

stroke (diagnosed clinically). He had a Glasgow Coma Score of 6 before being intubated. Outline your

management strategy for him for the first 24 hours.

[ Hide Answer ]

College Answer

Key Features

Obvious aention to ABC.

a) Urgency is required for the best results here. .

b) Investigation: CTA scan of brainstem to exclude a bleed (Although not the best investigation

compared to a MRI, but quickest and easiest to arrange) and to elucidate the vascular supply. Plus

exclusion of an embolic cause ie TOE should be done.

c) erapy: Discussion with neurologist/interventional neuroradiologist re urgent regional

thrombolysis/ angioplasty / platelet antagonists. .

d) Discussion with family re therapy and outlook.

Discussion

is brainstem stroke question is another one of these "outline your management" questions, where one

ought to go through a stereotypical pathway. Yes, you would direct your aention to the A B Cs and you

would maintain airway patency, ensure normoxia and normocapnea with mechanical ventilation, etc etc.

Ultimately, it is not the general supportive management which is the real question here. e college - I

assume - wants to know how well you understand the management of stroke. is topic is well explored

elsewhere.

Aer the airway has been controlled, the ventilation managed and the circulation appropriately supported,

one needs to establish whether this patient has had an embolic stroke (from his AF) or whether there has

been a haemorrhage. is is best done with a non-contrast CT brain.

If a haemorrhage has developed, giving features of brainstem pathology, it must be a central one, or one

which is extensive. In any case, hydrocephalus may develop, and one would get on the phone to the

neurosurgeons to get an EVD in, if not to evacuate the bastard. Surely the earlier this is done the beer.

If there is no haemorrhage, there is no point debating whether the stroke is embolic or ischaemic. One

would give thrombolysis immediately. e evidence for this is discussed elsewhere. Suffice to say, we give

people alteplase because the NINDS Study demonstrated a neurological recovery benefit without any

Home » CICM Fellowship Exam » Past Papers » 2006, Paper 2 SAQs

estion 26

increased bleed-related mortality. Mechanical embolectomy is an option if thrombolysis is contraindicated,

but it is a poorer option, and not as well supported.

en, the next 24 hours will be spent in anxious anticipation of a killing-blow intracranial bleed (as with

thrombolysis) or recovering from neurosurgical evacuation and EVD insertion. In either case, one ought to

have a word with the next of kin, so as to manage their expectations.

ough not immediately indicated, a carotid doppler and TOE should be performed to determine whether

the carotid artery or the fibrillating atrium are sources of the clot.

References:

Chapter 51 (pp. 568) by Bernard Riley and earina de Beer.

e Internet Stroke Centre has an excellent summary of stroke syndromes.

Kammersgaard, Lars Peter, et al. "Short-and long-term prognosis for very old stroke patients. e

Copenhagen Stroke Study." Age and Ageing 33.2 (2004): 149-154.

National Collaborating Centre for Chronic Conditions (Great Britain). "Stroke: national clinical guideline

for diagnosis and initial management of acute stroke and transient ischaemic aack (TIA)." Royal College of

Physicians, 2008.

Friedman, Howard S., W. J. Koroshetz, and N. reshi. "Tissue plasminogen activator for acute ischemic

stroke." N Engl J Med. 1995;333(24):1581.

A 42-year-old male presented with a stroke. He was admied to a general ward with a right sided

hemiplegia, neglect and speech deficits. e day following admission, you are called to the ward because

the patient has just become drowsy, and is no longer following commands. e team has performed a CT

scan of the head and this shows extensive le middle cerebral artery territory infarction, with no

haemorrhage, and early evidence of raised intracranial pressure.

a) Outline your initial plan of management. e family asks if there is any surgical option to “save” the

patient.

b) What is the evidence for surgery in this situation, and how would you advise the family?

[ Hide Answer ]

College Answer

a) e patient should be admied to an intensive care or stroke unit for close monitoring and

comprehensive treatment.

Transfer to a higher level centre is reasonable if comprehensive care and timely neurosurgical intervention

is not available locally.

Maintain SpO2 >95% - any safe comments or values.

Intubate if usual concerns regarding airway protection in neurologically impaired patient.

“Safe” blood pressure (Extreme hypertension associated with haemorrhagic transformation.

Concerned about malignant brain swelling with possible temporal herniation and the need to reduce the

space occupying effects of that swelling.

a) Elevate the head of the bed to 30°.

b) Do not hyperventilate PaCO2 35-40 mmHg

c) Increase levels of sedation +/- paralysis:

d) Barbiturate infusion – option, but not advocated in guidelines.

e) Osmotic therapy:

a. 3% Saline 100-200mL aliquots; Na+ ≤155mmol/L

b. Mannitol 0.5-1.0g/kg

c. Aim for serum Osm 300-320mOsm/L

) Target normoglycaemia

g) Hypothermia- temperature 35-36.5oC

Home » CICM Fellowship Exam » Past Papers » 2014, Paper 2 SAQs

estion 2

a. Prospective randomized studies are currently underway to further evaluate therapeutic hypothermia in

patients with cerebral infarcts.

b) Evidence

a. ree prospective, randomized trials (i.e. DESTINY, DECIMAL and HAMLET)

Supratentorial infarctions treated with decompressive craniectomy, usually within 48hours of stroke onset. Age <60. Older populations being currently studied.With hemicraniectomy compared with medical management:

Reduced mortality (22% versus 71% - pooled analysis)No individual study showed an improvement in the percentage of survivors with goodoutcomes (mRS score, 0–3),

Only shown in a pooled analysis (43% versus 21%).Only 14% of surgical survivors could look aer their own affairs without assistance(mRS score, 2)

Note:Names / excessive detail of studies not expected

Advice

I. e patient’s age <60 fits the studies’ inclusion criteria

II. Decompressive craniectomy for supratentorial infarction with swelling results in a

reproducible large reduction in mortality.

But mortality aer large ischaemic strokes with cerebral oedema remains between 20% & 30%despite medical and surgical interventions.Nearly all post-surgery survivors suffer residual permanent disabilities:

One half are severely disabledA third are fully dependent on care50% will suffer from depression

III. ere may be a discrepancy between physical disability and quality of life, with many patients and

families rating a good quality of life despite severe functional handicap. Ultimate advice and decisions will

be based on a balance between survival and level of disability.

Additional Examiners’ Comments:Candidates did not accurately read the question. Answers re advice to the family were not at the requiredlevel of sophistication.

Discussion

A systematic approach is called for.

a) is a question regarding the generic management of raised intracranial pressure, as well as the general

supportive management of acute stroke, which are topics well discussed elsewhere.

e brief point-form summary of management recommendations offered below is based completly on the

2014 AHA/ASA guidelines - "Recommendations for the Management of Cerebral and Cerebellar Infarction

With Swelling".

Admin) - e availability of a specialist acute stroke unit improves mortality and outcome; admission to

ICU does not (perhaps the opposite)

A) - intubate them to protect from aspiration (though it does not improve outcome)

B) - Ventilate aiming for a CO2 ~35mmHg (no evidence for or against hyperventilation, but the guidelines

statements tend to recommend a normal CO2)

C) - Tolerate a systolic blood pressure under 220mmHg systolic, or 120mmHg diastolic. (the evidence for

this is also not very robust)

D) - ere does not seem to be any point in monitoring the ICP. Rarely is the intracranial pressure raised. If

it were truly raised, the usual armamentarium of methods can be deployed.

E) Control hypeglycaemia, but not aggressively - tolerate borderline-high normoglycaemia.

F) Ensure normovolaemia and good hydration.

G) Ensure adequate nutrition, preferably by the enteric route.

H) No evidence to support the use of heparin infusion.

I) no strong evidence to support the use of therapeutic hypothermia.

b) e evidence for surgery (i.e. decompressive craniectomy in malignant MCA syndrome) is discussed in

detail elsewhere. In brief, the college model answer refer to three landmark studies:

DESTINY trial (2007)DECIMAL trial (2007)

HAMLET trial (2009)

A fourth could be mentioned: DESTINY II Trial (2014)

A pooled analysis of the first three studies is available, including 93 patient cases.

"…aer decompressive surgery the probability of survival increases from 28% to nearly 80% and theprobability of survival with an mRS of ≤3 doubles."

(mRS of 3 here being the score of the modified Rankin scale, equating to a disability where one requires

some help, some of the time, with some things - but is otherwise able to walk unassisted).

For advice to the family, the college quotes the AHA/ASA guidelines verbatim (see page 10):

"Decompressive craniectomy … results in a reproducible large reduction in mortality, butnearly all survivors suffer residual permanent disabilities.""No individual study showed an improvement in the percentage of survivors with goodoutcomes""Only 14% of surgical survivors could look aer their own affairs without assistance"

References:

: Chapter 51 (pp. 568) by

Bernard Riley and earina de Beer.

Torbey, Michel T., et al. "Evidence-Based Guidelines for the Management of Large Hemispheric

Infarction." Neurocritical care (2015): 1-19.

Wartenberg, Katja E. "Malignant middle cerebral artery infarction." Current opinion in critical care 18.2

(2012): 152-163.

Yang, Ming-Hao, et al. "Decompressive hemicraniectomy in patients with malignant middle cerebral artery

infarction: A systematic review and meta-analysis." e Surgeon (2015).

Jüler, Eric, et al. "Decompressive surgery for the treatment of malignant infarction of the middle cerebral

artery (DESTINY) a randomized, controlled trial." Stroke 38.9 (2007): 2518-2525.

Jüler, Eric, et al. "DESTINY II: DEcompressive Surgery for the Treatment of malignant INfarction of the

middle cerebral arterY II." International Journal of Stroke 6.1 (2011): 79-86.

Vahedi, Katayoun, et al. "Sequential-design, multicenter, randomized, controlled trial of early

decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial)." Stroke 38.9

(2007): 2506-2517.

Hofmeijer, Jeannee, et al. "Surgical decompression for space-occupying cerebral infarction (the

Hemicraniectomy Aer Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]):

a multicentre, open, randomised trial." e Lancet Neurology 8.4 (2009): 326-333.

Vahedi, Katayoun, et al. "Early decompressive surgery in malignant infarction of the middle cerebral artery:

a pooled analysis of three randomised controlled trials." e Lancet Neurology 6.3 (2007): 215-222.

Sloy, Philipp Jörg, et al. "e influence of decompressive craniectomy for major stroke on early cerebral

perfusion." Journal of neurosurgery (2015): 1-6.

Barroso, Bruno. "Decompressive craniectomy for stroke aer intravenous thrombolytic

therapy." International Journal of Stroke 9.8 (2014): E40-E40.

Wijdicks, Eelco FM, et al. "Recommendations for the Management of Cerebral and Cerebellar Infarction

With Swelling A Statement for Healthcare Professionals From the American Heart Association/American

Stroke Association." Stroke 45.4 (2014): 1222-1238.

Jüler, Eric, et al. "Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke." NewEngland Journal of Medicine 370.12 (2014): 1091-1100.

A 60-year-old male presents 2 hours aer the onset of vertigo and loss of consciousness. CT brain is

performed and shows right basilar and vertebral occlusion with no evidence of infarction.

Discuss two possible definitive treatment strategies for this condition, including the indications and contra-

indications of each.

[ Hide Answer ]

College Answer

TWO of the following:

Intravenous thrombolysis

e patient is within the suggested time window for thrombolysis and by current guidelines should receive

intravenous rtPA. Overall this treatment reduces deaths and dependency but is associated with a risk of

potentially fatal intracranial haemorrhage.

Indications include patients with acute ischaemic stroke presenting within the appropriate time window

(note to examiners – while initial guidelines suggested a time window of three hours there is data

suggesting use up to 4.5 hours may be beneficial)

Contraindications include:

Stroke or head trauma in previous 3 monthsIntracranial haemorrhage: past or presentMajor surgery in previous 14 daysGI or urinary tract bleeding in previous 21 daysMI in previous 3 monthsNon-compressible arterial puncture in previous 7 daysPersistent severe hypertensionActive bleeding or acute traumarombocytopaenia

Intra-arterial thrombolysis

Although intra-arterial thrombolysis results in higher rates of re-cannulation there is no evidence that it

reduces mortality or morbidity. However in patients who have undergone recent surgery (and therefore

have a contra-indication to intravenous thrombolysis) or exceed the 6 hour time window for intravenous

thrombolysis intra-arterial thrombolysis may be useful

Endovascular rombectomy

is technique may be used in large vessel thrombus,especially if recanalisation has not occurred with

intravenous thrombolysis, or the patient is outside the time window . It requires specialist expertise that

may not be generally available, and carries the risk of vascular damage or dissection with potential

worsening of symptoms.

Home » CICM Fellowship Exam » Past Papers » 2013, Paper 1 SAQs

estion 22

Indications would include ischaemic stroke in a large vessel in patients who have either failed thrombolysis

or have a contraindication to it.

Contraindications include:

Tortuous vessels precluding angiographic accessPre exisiting coagulopathyEstablished infarct on imagingContrast allergy

Discussion

In essence, a stroke patient presents well within the timeframe for reperfusion therapy.

Let us tabulate this answer.

Management Options for an Early Presentation of Ischaemic Stroke

Intravenousrombolysis

Presentation within 3 hoursAge over 18 and less than 80

History of head trauma in the last 3 monthsHistory of stroke in the previous 3 monthsArterial puncture in a non-compressible site in thepast 7 daysPlatelet count less than 100Any heparin within 48 hours of the strokeCurrent anticoagulant therapyHypoglycaemiaMultilobar infarction (more than one-third of acerebral hemisphere) on CT scan

Intraarterialthrombolysis

Contraindication to systemicthrombolysisSystemic thrombolysis is consideredlikely to failSystemic thrombolysis has failed(aer 1 hr)A large vessel occlusion is present

Poor vascular accessIntracerebral haemorrhageCerebral malignancy (relative)

Endovascularembolectomy

Presentation within 8 hoursContraindication to systemicthrombolysis (or failure to respond toit)Clot is in a large vessel

Contraindications to carotid or verterbal arterialaccess (eg. significant carotid atherosclerosis)Peripheral vascular disease (i.e. difficult access)Uncontrolled coagulopathyObvious and well-established infact on CT or MRI(thus, no point in embolectomy)Contrast allergy

e MERCI trial investigators managed to get good outcomes even 8 hours post infarct, which is

encouraging. However, these outcomes were still poorer than historical controls.

e issue of acute stroke management is discussed in brief summary elsewhere.

References:

: Chapter 51 (pp. 568) by Bernard

Riley and earina de Beer.

Smith, Wade S., et al. "Safety and efficacy of mechanical embolectomy in acute ischemic stroke results of

the MERCI trial." Stroke 36.7 (2005): 1432-1438.

Nogueira, R. G., et al. "Endovascular approaches to acute stroke, part 2: a comprehensive review of studies

and trials." American Journal of Neuroradiology30.5 (2009): 859-875.

Brinjikji, Waleed, et al. "Patient outcomes with endovascular embolectomy therapy for acute ischemic

stroke a study of the national inpatient sample: 2006 to 2008." Stroke 42.6 (2011): 1648-1652.

Kidwell, Chelsea S., et al. "Design and rationale of the mechanical retrieval and recanalization of stroke

clots using embolectomy (mr rescue) trial."International Journal of Stroke 9.1 (2014): 110-116.

Jansen, Olav, et al. "Neurothrombectomy for the treatment of acute ischemic stroke: results from the

TREVO study." Cerebrovascular Diseases 36.3 (2013): 218-225.

Furlan, Anthony, et al. "Intra-arterial prourokinase for acute ischemic stroke: the PROACT II study: a

randomized controlled trial." Jama 282.21 (1999): 2003-2011.

Sacks, David, et al. "Multisociety consensus quality improvement guidelines for intraarterial catheter‐

directed treatment of acute ischemic stroke, from the American Society of Neuroradiology, Canadian

Interventional Radiology Association, Cardiovascular and Interventional Radiological Society of Europe,

Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of

NeuroInterventional Surgery, European Society of Minimally Invasive Neurological erapy, and Society of

Vascular and …." Catheterization and Cardiovascular Interventions 82.2 (2013): E52-E68.

Ogawa, Akira, et al. "Randomized trial of intraarterial infusion of urokinase within 6 hours of middle

cerebral artery stroke e Middle Cerebral Artery Embolism Local Fibrinolytic Intervention Trial (MELT)

Japan." Stroke 38.10 (2007): 2633-2639.

Outline the advantages and disadvantages of the various techniques used in the diagnosis and monitoring

of vasospasm secondary to aneurysmal subarachnoid haemorrhage.

[ Hide Answer ]

College Answer

Techniques that have proven or demonstrated potential in the diagnosis and monitoring of

vasospasm include:

In the conscious patient, may be detected clinically by new focal neurology or a drop in GCS. Advantages:

No additional costs and readily available, can be repeated easily, non-invasive (usually), has to be

performed at the bedside. Major disadvantage is lack of specificity oen necessitating CT/angiography.

Also lacks sensitivity, vasospasm can occur without a clinical correlate, early in the disease. Operator

dependent.

Remains the gold standard for diagnosis of vasospasm.

May allow therapeutic intervention (angioplasty) at the time.

Disadvantages: invasive, risks of bleeding, embolism, radiation/contrast exposure and transport. Requires

skilled interventional radiology, and therefore resource heavy. Risk of stroke (quoted about 1%, but

probably a lile lower) just from the angio, plus the dissections etc. that occur as well.

Detects vessel narrowing, not necessarily poor flow to distal tissue in all cases (either increased flow rate

through narrow vessel or collateral supply. May lead to over treatment.

It is low risk, performed at the bedside, non-invasive and able to be repeated daily enabling trend

analysis.

Disadvantages:

e technique is however operator dependent and there is high inter- observer variability. Debate exists regarding correlation of flow velocity and vasospasm and although highvelocities (> 200cm/sec) are predictive, lower velocity may not be as good.e technique may be more accurate when MCA velocity is indexed to the ipsilateralextracranial carotid artery (Lindegaard index, >3 strongly predictive). Colour coded TCD may offer greater accuracy than plain TCD alone.

May be combined with perfusion allowing characterisation of both vascular anatomy andassociated perfusion abnormalities.

Home » CICM Fellowship Exam » Past Papers » 2013, Paper 2 SAQs

estion 2

MR diffusion weighted imaging accurately identifies brain tissue at high risk of infarction;perfusion weighted imaging reveals asymmetries in regional perfusion. Both methods show correlation with delayed ischaemic neurological deficit (DIND). Disadvantages:

Image clarity will be affected by clip/coil and contrast related issues need consideration.e overall diagnostic capability of this modality however remains unclear until furtherprospective studies are performed. Similar disadvantages as per angiography with respectto transport, radiation (for CT), contrast exposure, interpretation by experts.

Can be used to obtain a picture of brain perfusion and metabolism and have shown variable correlation with vasospasm as assessed by more conventional methods.Disadvantages: ey are resource heavy not easily available, radiation exposure, patient transport are issues.

May provide prognostic information, focal areas of slowing correlate with angiographicvasospasm and a decrease in alpha to delta ratio strongly correlates with ischaemia. Sensitivityand specificity for detecting vasospasm is high.

Disadvantage: Not readily available however and their may be issues with

interpretation.

e use of measures of tissue oxygenation using parenchymal sensors and microdialysis for monitoring biochemical indices of ischaemia are largely research tools.

Salient pointsClinical examinationDSACTAEEGTranscranial dopplerParenchymal sensorsSPECT

Discussion

is answer lends itself well to a table format.

Clinicalexamination

CheapAvailable at the bedsideEasily sequentialised

InaccurateOperator-dependentMany episodes of vasospasm are notassociated with physical signs

DSA Gold standardOffers a means of treating the vasospasm

May overtreat by picking up narrowingwhich is not associated with a decreased flowRadiation exposureContrast exposureNeed for transportNeed for skilled personnelinvasive1% risk of stroke or dissection

CTA Reasonable sensitivity and specificityNon-invasive

Radiation exposureContrast exposureNeed for transportNeed for skilled personnel

Frustrated by the presence of coils and clips(artifact is generated)

Transcranial

Doppler

High (100%) specificity;non invasiveEasily sequentialised

Operator-dependentMediocre sensitivity

EEG Highly sensitive and specificCan pick up features of ischaemia andvasospasm earlier than the developmentof obvious signs or radiological featuresNon invasive

Requires skilled operator and interpreter;may not be availableIdeally, EEG monitoring should becontinuous.

SPECT potentially very useful in detectingischaemia and cerebral hypoperfusion

Not validated, and mainly a tool of research

Apocryphal notes on the diagnosis and management of SAH are also available.

References:

Chapter 51 (pp. 568) by Bernard Riley and earina de Beer

Marshall, Sco A., Paul Nyquist, and Wendy C. Ziai. "e role of transcranial Doppler ultrasonography in

the diagnosis and management of vasospasm aer aneurysmal subarachnoid hemorrhage." NeurosurgeryClinics of North America21.2 (2010): 291-303.

Greenberg, E. D., et al. "Diagnostic accuracy of CT angiography and CT perfusion for cerebral vasospasm: a

meta-analysis." American Journal of Neuroradiology 31.10 (2010): 1853-1860.

Sloan, M. A., et al. "Sensitivity and specificity of transcranial Doppler ultrasonography in the diagnosis of

vasospasm following subarachnoid hemorrhage." Neurology 39.11 (1989): 1514-1514.

Rivierez, M., et al. "Value of electroencephalogram in prediction and diagnosis of vasospasm aer

intracranial aneurysm rupture." Acta neurochirurgica 110.1-2 (1991): 17-23.

Critically evaluate the current approaches to the treatment of cerebral vasospasm following aneurysmal

subarachnoid haemorrhage.

[ Hide Answer ]

College Answer

Treatment

b) Triple H therapy-HT, hypervolemia and hemodilution-controversial, not evidence based

c) Early clipping / coiling

d) Nimodipine -useful in prophylaxis,

e) Endoluminal·therapies: Balloon angioplasty and intra-arterial papaverine

Investigational therapies -proven in animal models, no hard clinical evidence, no RCT

1) Statins-Early human data

2) Cisternal tPa

3) Endothelin antagonists

Discussion

is topic is well developed in the chapter on subarachnoid haemorrhage.

True to the college answer, there is only strong evidence for nimodipine and endovascular vasodilators. Of

the "triple-H" therapy, the only evidence-based component is probably hypertension, and even this is being

debated.

Judging by the college answer, they did not want a discussion of Class I recommendations from highly

regarded advisory bodies. e model answer mentions some wacky "failed therapies" for vasospasm which

have subsequently receded into historical background noise.

In summary:

Once vasospasm is suspected, DSA (the gold standard investigation) should be performed.On DSA, one can access the vessels involved and inject intra-arterial papaverine or verapimil.Nimodipine is the only preventative pharmacotherapy supported by evidence. e BRANTtrial from England has demonstrated a 34% decrease in the risk of SAH-induced stroke.Of the "Triple H" circulating volume expansion strategies, only hypertension persists as a validtreatment - and it is only supported by a consensus of neurosurgeons.

"Triple H therapy" in general- i.e. prophylactic hypertension, haemodilution andhypervolaemia - has lile to recommend it. Myburgh was already tearing shreds out of it in2005.

Home » CICM Fellowship Exam » Past Papers » 2007, Paper 1 SAQs

estion 10

Intrathecal thrombolysis is promising, but not well supported - a 2004 Japanese study foundintrathecal urokinase decreased the incidence of vasospasm by almost 50%.Statins - no benefit (STASH trial)Endothelin 1 antagonists (eg. clazosentan) - no strong support, perhaps some subtle benefit(CONSCIOUS-1 trial)Magnesium – no benefit (MASH-2 trial)Tirilazad - a non-glucocorticoid aminosteroid that blocks lipid peroxidation - fiver RCTs; onlyone showed any benefit, and its efect was lost in the noise accoridng to a Cochrane meta-analysis.Fasudil - a Rho kinase inhibitor that prevents the effects of extracellular calcium on smoothmuscle contraction - promising on the basis of 8 RCTs, but still not fully supported by theevidence according to a 2012 meta-analysis.Eicosapentaenoic acid - which also inhibits Rho kinase, like fasudil - promising results of onesmall study (the EVAS trial); thus far it still falls into the "experimental" category.

References:

Connolly, E. Sander, et al. "Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage A

Guideline for Healthcare Professionals From the American Heart Association/American Stroke

Association." Stroke 43.6 (2012): 1711-1737.

Myburgh, J. A. "Triple h” therapy for aneurysmal subarachnoid haemorrhage: real therapy or chasing

numbers." Crit Care Resusc 7.3 (2005): 206-212.

Bederson, Joshua B., et al. "Guidelines for the management of aneurysmal subarachnoid hemorrhage a

statement for healthcare professionals from a special Writing Group of the Stroke Council, American Heart

Association."Stroke 40.3 (2009): 994-1025.

Kawamoto, Shunsuke, et al. "Effectiveness of the head-shaking method combined with cisternal irrigation

with urokinase in preventing cerebral vasospasm aer subarachnoid hemorrhage." Journal ofneurosurgery 100.2 (2004): 236-243.

Vergouwen, Mervyn DI, et al. "Biologic effects of simvastatin in patients with aneurysmal subarachnoid

hemorrhage: a double-blind, placebo-controlled randomized trial." Journal of Cerebral Blood Flow &Metabolism 29.8 (2009): 1444-1453.

Macdonald, R. Loch, et al. "Clazosentan to Overcome Neurological Ischemia and Infarction Occurring Aer

Subarachnoid Hemorrhage (CONSCIOUS-1) Randomized, Double-Blind, Placebo-Controlled Phase 2 Dose-

Finding Trial."Stroke 39.11 (2008): 3015-3021.

Examine the single slice non-contrast CT image, depicted below, of a 58-year-old male who was brought to

the Emergency Department with a headache. He was not on any medication.

a) Name the structures labelled A- E.

b) Describe lesion F as you would on the phone to a neurosurgical colleague.

c) Give three pathological causes for F.

A day aer the CT scan the patient's Glasgow Coma Scale drops from 13 to 10.

d) Give three possible intracranial causes for this.

e) List five validated features affecting prognosis for patients with F.

[ Hide Answer ]

College Answer

Home » CICM Fellowship Exam » Past Papers » 2014, Paper 1 SAQs

estion 25

a)

A Le frontal cortex

B Caudate nucleus

C Top of quadrigeminal cistern (not 3rd or 4th ventricle)

D Septum pellucidum

E Posterior horn of le lateral ventricle

b)

'Acceptable' answer:

ere is a hyperdensity in keeping with an intracerebral haematoma in the right frontoparietal region with

midline shi and surrounding oedema.

c)

Hypertensive haemorrhage.

AV malformation.

Haemorrhagic transformation of ischaemic stroke.

Bleed into tumour.

(No evidence of subarachnoid haemorrhage).

d)

Expanding haematoma / Worsening oedema / mass effect.

Seizure (including non-convulsive).

Hypdrocephalus due to obstruction of ventricles.

e)

e features included in the intracerebral haemorrhage score are:

Age: < 80 or > 80

GCS: on transfer from the ED to definitive to care.

Location of bleed: supra vs infra tentorial.

Volume of Bleed: < 30 mL or > 30 mL.

Intraventricular extension of haemorrhage.

Discussion

e image above is not the gospel CICM image, but was stolen shamelessly from a 2009 article by Jae-Suk

Park et al.

e answers to a), b), c) and d) should be a part of an ICU trainee's reptilian hindbrain activity.

If one's cross-sectional neuroanatomy was for some reason sub-optimal, one could pay a visit to the

excellent wikiradiography Head CT page.

Differential explanations for "a hyperdensity in keeping with an intracerebral haematoma" are:

Intracerebral haematoma, due to

Hypertension

Potentially associated with abuse of stimulants, eg.cocaine

Amyloid angiopathyArteriovenous malformationIntracranial aneurysm (though there is no subarachnoid blood)Cavernous angiomaVenous angiomaDural venous sinus thrombosisHaemorrhage into the intracranial neoplasmHaemorrhage into an ischaemic stroke (haemorrhagic transformation)Vasculitis

is list of differentials was retrieved from an excellent 2001 NEJM article by Adnan reshi.

e college then asks for five validated features which affect prognosis. Fortunately, an article

titled"Development and validation of the Essen intracerebral haemorrhage score" can rescue us from

wondering what hidden meaning the College had concealed within the remark I italicised. Presumably, the

examiner behind it is also aware of, and perhaps is mildly annoyed by, several published prognostic

features for ICH which are completely unvalidated.

e specific scoring system referred to in the official model answer was probably the modified Essen ICH

score rather than the original ICH score. One can view the original system here and Essen scoring

system here. Detailed familiarity with them is not essential; however one should recall that the following

variables suggest a poor prognosis:

Age over 80A high NIH-SS score (National Institutes of Health stroke scale)GCS (3-4)Volume of blood exceeding 30ml (30cm2)Infratentorial originIntraventricular extension of haemorrhage

References:

Park, Jae-Suk, et al. "Remote cerebellar hemorrhage complicated aer supratentorial surgery: retrospective

study with review of articles." Journal of Korean Neurosurgical Society 46.2 (2009): 136-143.

reshi, Adnan I., et al. "Spontaneous intracerebral hemorrhage." New England Journal of Medicine 344.19

(2001): 1450-1460.

Hemphill, J. Claude, et al. "e ICH score a simple, reliable grading scale for intracerebral

hemorrhage." Stroke 32.4 (2001): 891-897.

Weimar, Christian, Jens Benemann, and H. C. Diener. "Development and validation of the Essen

intracerebral haemorrhage score." Journal of Neurology, Neurosurgery & Psychiatry 77.5 (2006): 601-605.

Rost, Natalia S., et al. "Prediction of Functional Outcome in Patients With Primary Intracerebral

Hemorrhage e FUNC Score." Stroke 39.8 (2008): 2304-2309.

Garre, John S., et al. "Validation of Clinical Prediction Scores in Patients with Primary Intracerebral

Hemorrhage." Neurocritical care 19.3 (2013): 329-335.

Compare and contrast the advantages and disadvantages of coiling versus clipping of cerebral

aneurysms aer Sub-Arachnoid Haemorrhage.

[ Hide Answer ]

College Answer

Recent published experience demonstrates that there are some significant potential benefits associated with

coiling of cerebral aneurysms. ese include decreased costs, no need for craniotomy and associated

neuroanaesthetic, and increased independent survival (“ISAT” Lancet 2002; 360:1267-74). Other potential

advantages include no need for temporary clipping. Major disadvantages include the need for a skilled

operator, the fact that technique is not suitable for all aneurysms, requirement for anticoagulation, and

inability to deal with major complications. A neurosurgical procedure may still be required if

complications ensue.

Clipping has a long track record with clearly defined risks, with no evidence of increased mortality. Most

aneurysms are amenable to clipping, though in some regions (eg. posterior fossa), because of accessibility,

coiling is considered the procedure of choice. Disadvantages of surgical clipping include need for a skilled

operator, a craniotomy and neuroanaesthesia, and potentially increased costs.

Both techniques require some degree of sedation/paralysis, and subsequent neuro-Intensive care with close

monitoring and re-evaluation for complications. Either technique may be quite prolonged.

Discussion

e coiling vs clipping debate is aired briefly in the chapter on management of the unsecured aneurysm in

subarachnoid haemorrhage. In it, there is this table:

Coiling vs clipping in ruptured aneurysms

minimally invasiveimproved survival at 1 yearBeer effects in posterior fossa aneurysmsLess risk of cognitive decline or epilepsy

More certain: 81% of aneurysms are completelyobliteratedLess risk of rebleeding (0.9%)MCA aneurysms are more amenable to clipping

Greater risk of rebleeding (2.9%)Fewer aneurysms get completely obliterated (58%)Small aneurysms (<3mm) are impossible to coil

More invasiveGreater risk of cognitive decline or epilepsySurvival rates equivalent at 5 yearsPosterior fossa aneurysms are inaccesible to clipping

Home » CICM Fellowship Exam » Past Papers » 2005, Paper 1 SAQs

estion 16

References:

Bakker, Nicolaas A., et al. "International subarachnoid aneurysm trial 2009: endovascular coiling of

ruptured intracranial aneurysms has no significant advantage over neurosurgical

clipping." Neurosurgery 66.5 (2010): 961-962.

Connolly, E. Sander, et al. "Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage A

Guideline for Healthcare Professionals From the American Heart Association/American Stroke

Association." Stroke 43.6 (2012): 1711-1737.

With respect to pathological conditions of the spinal cord, for each of the following syndromes, list

two causes and the clinical findings:

Complete cord transectionCord hemisectionCentral cord syndromeAnterior cord syndrome (anterior spinal artery syndrome)Cauda Equina syndrome

(You may tabulate your answer.)

(20% marks per syndrome)

[ Hide Answer ]

College Answer

Complete Transection Trauma, Infarction, Transversemyelitis, Abscess, Tumour

Complete loss of motor and sensoryfunction below level of the lesion

Cord Hemisection Trauma, Tumour, Multiplesclerosis, Abscess

Ipsilateral loss of motor andproprioception. Contralateral pain andtemperature loss

Central Cord Neck hyperextension,Syringomyelia, Tumour

Motor impairment greater in upperlimbs than lower Variable sensory loss,bladder dysfunction

Anterior Cord Hyperflexion, Disc protusion,Anterior spinal artery occlusion,Post AAA

Motor function impairment, Pain andtemperature loss, proprioceptionspared.

Cauda Equina Disc protusion, Tumour, Infection Bladder/bowel dysfunction Alteredsensation in saddle area, sexualdysfunction

Discussion

e Important spinal cord injury syndromes chapter from the Required Reading section contains a table of

spinal cord injury syndromes, which is reproduced below to simplify revision.

In brief:

contains motor tracts; anterior cord damage results in motor paralysis withpreserved sensation.

contains predominantly sensory tracts, and damage there will result inpredominantly sensory loss, with preserved movement.

contains ipsilateral motor/ proprioception and contralateral pain /temperature fibers. Damage there will leave the damaged side paralysed, and the opposite side

Home » CICM Fellowship Exam » Past Papers » 2015, Paper 1 SAQs

estion 15

anaesthetised.contains motor fibers from the upper limb (lower limb fibers are more

peripheral). Damage there will cause upper limb paralysis.governs lower limbs, bladder and bowel. Saddle anaesthesia is the key

feature.

Causes and Characteristic Features of Spinal Cord Syndromes

ere are some causes which are generic for all these syndromes, and they will not be repeated in each box. ese are:

TraumaInfarctionAbscess

Tumour or metastatic compressionHaematomaAVM/haemorrhage

Any of these can cause any of the spinal syndromes, anywhere. Instead of these, the causes listed below are the

characteristic pathological processes which usually give rise to a specific spinal cord syndrome, eg. anterior spinal

artery occlusion causing anterior spinal syndrome.

Cord transection Lost bilateral motorFlaccid areflexiaLost bilateral sensory

Usually traumaTransverse Myelitis

Cord hemisection Lost ipsilateral motorLost ipsilateral proprioceptionLost ipsilateral light touchLost contralateral pain and temperature

Penetrating spinal injuryRadiation inurySpinal metastases

Anterior cord injury Preserved bilateral proproceptionLost bilateral pain, temperature, touchLost bilateral motor control

Interruption of the blood supply to the

anterior spinal cord:

Aortic dissectionIABP complication

Posterior cord injury Lost proprioceptionOther sensation preserved bilaterallyPreserved power bilaterallyAtaxia results

Hyperextension injuryPosterior spinal artery injuryTertiary syphilisFriedrich's ataxiaSubacute degeneration (Vitamin B12deficiency)Atlantoaxial subluxation

Central cord syndrome Sacral sensation preservedGreater weakness in the upper limbsthan in the lower limbs.

Hyperextension injury with pre-existing canal stenosisEpendymomaSyringomyelia

Conus medullaris syndrome symmetrical paraplegiaMixed upper and lower motor neuronfindings

e same sort of pathologies cangive rise either to a cauda equinasyndrome or a conus medullarissyndrome; the difference is the level.

Cauda Equina syndrome asymmetrical, lower motor neuronlower limb weaknesssaddle area paraesthesiabladder and bowel areflexia

Syndrome Characteristic features Causes

A 69-year-old man has been ventilated for an infective exacerbation of chronic obstructive pulmonary

disease (COPD). erapy has included steroids and an aminoglycoside antibiotic. His ICU course has been

complicated by septic shock and acute kidney injury.

Twelve days later neurological examination off sedation reveals moderate to severe weakness of his limbs

with intact sensation, normal cognition and normal cranial nerves

List the differential diagnoses for his weakness.Outline how you would determine the diagnosis.List of differential diagnoses for his weakness

[ Hide Answer ]

College Answer

a) List of differential diagnoses for his weakness

Critical illness myopathy / Acute quadriplegic myopathy* (high dose steroids, with orwithout nondepolarising paralyzing agent use, Beta agonists)

Critical Illness polyneuropathy/myopathy* (SIRS, sepsis, MODS)*Residual sedation and other drug influences (Renal [&/or liver] impairment contributing, aminoglycoside with NMJeffect)

*Electrolyte abnormalities (PO4, Ca++, K+)Deconditioning with weakness exacerbated by subclinical sepsisUnderlying polyneuropathy/myopathy exacerbated by critical illness Alcohol, B12 deficiency,paraneoplastic, consider diabeticGBSRhabdomyolysis (drugs (e.g. statins), infections) should be thought of given renal failureacute myelitis or watershed infarction (acute upper motor neuron lesions may not yet havedeveloped hypertonia and hyper-reflexia)Autoimmune neuropathy or myopathy (rare)

b) Diagnosis

Any relevant history.

Clinical examination:

Normal higher functions and cranial nerves favour a critical illness neuromyopathy(CINM) or a purely peripheral nervous system. Spinal lesion possible although less likely+ normal sensory examinationSymmetrical features on peripheral neurological exam also favours CINM. Cerebralwatershed infarction is possible but less likely given distal power is usually relativelyspared.Critical illness myopathy oen affects the diaphragmTendon reflexes are absent or profoundly decreased in neuropathies and decreased inmyopathies. ey should be essentially normal in de-conditioning or with residualsedative effect.Plantars are unhelpful as they are equivocalLack of focal neurology or relative sparing of distal motor power (watershed infarction)tends to exclude central causes (eg CVA) or mononeuropathies.]

Home » CICM Fellowship Exam » Past Papers » 2012, Paper 1 SAQs

estion 25

Distribution of weakness is symmetrical in all other causes and tends to be moreprofound proximally in myopathies, facial involvement tends to occur more inmyopathies than in neuropathies (rare exception Miller-Fisher GBS variant).Muscle wasting may be present with myopathies and when there exists a pre-existingmyopathy or neuropathy. Muscle fasciculation is uncommon but if present supports alower motor neuron lesion, severe neuropathy or myopathy.

Investigations:

Check biochem and ABGs (U&E’s, LFT’s – espy K, PO4, Ca, Mg, pH, PaCO2), FBE andinflammatory markers, Vit D and Gentamicin levelReview cultures and sensitivities and abx used to determine the possibility of ongoing orresistant infection.CK – timing of test to be considered (Best done in first 7 days of illness – if not performedadd test to previous blood samples - Elevated in myopathiesNerve conduction studies and Electromyographic studies help support diagnoses ofneuropathy and myopathy (vs severe deconditioning or central causes)CSF analysis (GBS), may be required .Muscle Biopsy may be required.MRI if central cause suspected or NCS and EMG don’t support CINM

Discussion

e college answer is extensive and covers the territory well.

For revision purposes, several chapters exist locally:

Ch.5.5.1 - Approach to the ICU patient with generalised weaknessCh.5.5.2 - Features that distinguish myopathy from neuropathyCh.5.5.3 - Intensive Care for Guillain-Barre SyndromeCh.5.5.4 - Critical illness polyneuromyopathyCh.5.5.5 - Features that distinguish Guillain-Barre syndrome from critical illnesspolyneuromyopathy

From the above resources (specifically, from the table in chapter 5.5.1) I will pick some relevant conditions

and put them in a sensible paern to assist their recollection:

Central:

Spinal or brainstem ischaemia (unlikely)

Peripheral nerve:

Autoimmune polyneuropathy, eg. Guillain-Barre syndromeCriticial illness neuromyopathyNutritional polyneuropathy, eg. B12 deficiency

Neuromuscular junction

Myasthenia gravis (unlikely)Aminoglycoside-induced weakness (in association with neuromuscular junction blockers)

Muscle

Atophy due to prolonged ICU stay, hypercatabolic state and malnutritionCriticial illness neuromyopathySteroid myopathyElectrolyte derangement, eg. hypophosphataemia, hypocalcemia, hypermagnesemia orhypokalemia

GCS (brainstem-damaged or "locked in" syndrome)Gross bilateral power (looking for symmetry, distal sparing, lateralising motor feature)Cranial nerve examination (Normal cranial nerves suggest a purely peripheral problem)Tendon reflexes (absent in neuropathies, decreased in myopathies)Fatiguability (Myasthenia gravis vs. "reverse" fatiguability with Lambert-Eaton syndrome)

Electrolyte levelsCK levelB12 level

Inflammatory markersLumbar punctureNerve conduction studiesElectromyographyMRI of the brainstem and spineMuscle biopsy if no satisfactory explanation is found.

References:

:

Chapter 51 (pp. 568) by Bernard Riley and earina de Beer

Chapter 57 (pp. 617) by George Skowronski and Manoj

K Saxena

Yuki, Nobuhiro, and Hans-Peter Hartung. "Guillain–Barré syndrome." New England Journal ofMedicine 366.24 (2012): 2294-2304.

Jani, Charu. "Critical Illness Neuropathy." Medicine (2011): 237.

Young, G. Bryan, and Robert R. Hammond. "A stronger approach to weakness in the intensive care

unit." Critical care 8.6 (2004): 416.