nn 6 hof Hf*
onset.
Methods: Matched case-contiolstudyol SS patients
at 21 emergency departments between 2000 and
2011,and diagnoses were verified by LP.
Results: The clinical pied ci on rule fotdiagnosis
of SAH was 97.1% sen sitire.22.7% specific, and
tad a negative likelr
-wod ratio of 0.13. Using the
nagmg prediction rule resulted in a false negalne
rate of 20%.
Conclusions: Performing tte clinical and imag -g
rules together hasthe potential for maximizing
sensitivity of prediction and reducing rates of IP. but
using imaging alone can resell in missed cases.
Blood in
Sylvian fissures
Blood on
surface of tentorium
Figure 19. Diagnosis of SAH
Positive (NCCT}
s
03— (Positive)
rtf No CT or MRA
positive f
T
( Diagnostic PSA )
Gold Standard
( MRI/MRA ) ( LP ) C 1 J I
, l l
LP positive
Diagnostic DSA i
( OR
! .1 .1
The Vasograde:A Simple Grading Scale for
Prediction of Delayed Cerebral Ischemia after
Subarachnoid Hemorrhage
Stroke 2015;46|7):1826TJ31
Purpose: Patients are classically at risk of delayed
ceietual ischemia (OCI)aftei aneurysmal SAH.Ihis
study validated a grading scale-the VASOGRADE -
for prediction of DCI.
Methods: Oata from three Phase II RCTs and a s ogle
hospitalseries were used to assess the lelationshp
between the VASOGRADE and DCI.
Results: in a cohort of 746 patients, the VASOGRADE
significantly predicted Ml (P<0.001). lire
YASOGRADE-Yellow had a tendency lor increased risk
for DCI (OR 1.31:95% Cl 0.77-2.23) when compared
With VASOGRADE- Green:those with VASOGRAOE-Red
had a 3 fold higher tisk of DCI (OR 3.19;95% Cl 2.07-
4.50|.VASOGRADE had an adequate diswmuut c - foi
prediction of OCI {area under the receiver operating
characteristics cune-0.63) and good calibration.
Conclusions:Ire VASOGRADE results validated
previously published risk chartsin a large and
d versesample of SAH patients,which allows DCI risk
stiatdication on piesentalon after SAH.It coJd help
to select patients at fugh-nsk of OCI and standardize
treatment protocols and research studies.
to
x—> 6
— — r-
(Coiling) (Clipping)
'
r
( Stop ] ( Stop ] ( Slop )
Gold Standard
Figure 20. Approach to SAH
Adapted from:de Oliveira Manoel et al. (2014)Subarachnoid haemorrhage Irom a neuroimaging perspective.Critical Care
Treatment
•admit to K!U or NICU
oxygen/ventilation PRN
NPO, bed rest, elevate head of bed 30“, minimal external stimulation, neurological vitals ql h
• aim to maintain sBP=120-150 mmHg (balance of vasospasm prophylaxis, risk of rebleed, risk of
hypotension since CBF autoregulation impaired by SAH)
• cardiac rhythm monitor, Foley PRN,strict monitoring of ins and outs
•medications
IV NS with 20 mmol KC1/L at 125-150 cc/h
nimodipine 60 mg PO/NG q4 h x 21 d for delayed cerebral ischemia neuroprotection; may
discontinue earlier if patient is clinically well
seizure prophylaxis:levetiracetam (Keppra*) 500 mg PO/IV q12 h x 1 wk
• mild sedation PRN
• neuroprotection
the only validated neuroprotective agent is nimodipine
studies on the use of IV magnesium and endothelin-A receptor antagonist (clazosentan)showed
reduction in DCI and vasospasm, respectively, without any effect on functional outcome
a trial on the use of statins did not show any neuroprotective benefit
r -x
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Complications
• vasospasm:vasoconstriction and permanent pathological vascular changes in response to vessel
irritation by blood can lead to delayed cerebral ischemia and death
onset: 4-14 d post-SAH, peak at 6-8 d; most commonly due to SAH, rarely due to ICH/IVH
• clinical features(new onset ischemic deficit):confusion, decreased LOC,focal deficit (speech or
motor, e.g. pronator drift)
risk factors:large amount of blood on CT (high fisher grade),smoking,increased age, HT'
N
“symptomatic"vasospasm in 20-30% of SAH patients
“angiographic” vasospasm in 30-70% of arteriograms performed 7 d following SAH
diagnosed clinically, and/or with transcranial Doppler (increased velocity of blood flow)
risk of cerebral infarct and death
treatment
hyperdynamic (“triple H”) therapy using fluids and pressors, usually after ruptured
aneurysm has been clipped/coiled
direct vasodilation via angioplasty or intra-arterial verapamil for refractory cases
• delayed cerebral ischemia: neurological deterioration persisting >1 h in the absence of any obvious
contributing physiological,radiological, or laboratory abnormalities
peaks 4-10 d post-ictus
can progressto cerebral infarction and is associated with significant morbidity and mortality
• mechanism behind DG is unclear, hut includes vasospasm, vascular dysautoregulation,
neurotoxic effects from the blood breakdown products, inflammation, micro-thrombi, and
corticalspreading depolarizations
» it is an essential target for SAH management
• hydrocephalus(15-20%):due to blood obstructing arachnoid granulations
can be acute or chronic, requires extraventricular drain orshunt, respectively
• neurogenic pulmonary edema
• hyponatremia:due to cerebral salt wasting (increased renal sodium loss and EG;
volume loss), not
S1ADH
• Dl
• cardiac:arrhythmia (>50% have ECG changes), Ml,CHF
VASOGRADE
VASOGRAOi WFNS Modified
Fisher scale
Green M 1-2
Yellow 1-3 34
Red 45 Any
The Durability of Endovascular Coiling vs.
Neurosurgical Clipping of Ruptured Cerebral
A ncurysms:18 Yr Follow-Up of The U K Cohort
of the International Subarachnoid Aneurysm
Trial(ISM)
lancet 2015:385(9969):691-697
Methods: RCT comparing endovascular coiling
treatment with craniotomyand dipping for luptured
intracranial aneurysms in 2143 patients who were
considered eligible for either modality or therapy
between 1994-2002.1644 patients were Mowed lor
deaths and outcomesfor10-18.5 yr.
Results:At10 yr.83% of endovascular coiling group
and 79% of neurosurgical clipping groupwere alive.
82% of patientstreated with endovascular coiling and
78% of patients treated with neurosurgical dipping
were independent.Fatients m the endovascular
group were more likely to be alive and independent
at10 yr vs.neu rosurgery group (081.34,95% Cl
1.07-1.67). Rebleeding risks from target aneurysm for
endovascular group and neurosurgery groupwere
0.0216 (95% Cl 0.0121 0.0383) and 0.0064|95% CI
0.0024-0.0173),respectively..
Conclusions:
IThe probability of death or dependency was
significantly greater in the neurosurgical group (vs.
endovascular group) at10 yr follow-up.
2.Rebleeding was more likely in endovascular group
(vs. neurosurgical group), but risk wassaall at 10
yr follow-up.
3. Probability of disability-free survival was
significantly greater in the endovascular group (vs.
neurosurgical group) at 10 yt follow-up.
Prognosis
• 10-15% mortality before reaching hospital, overall 50% mortality (majority within first 2-3 wk)
• 30% ofsurvivors have moderate to severe disability'
• a major cause of mortality is rebleeding, for untreated aneurysms:
• risk of reblecd: 4% on 1st day, 15-20% within 2 wk, 50% by 6 mo
• if no rebleed by 6 mo, risk decreases to same incidence as unruptured aneurysm (2%)
• only prevention is early clipping or coiling of “cold" aneurysm
rebleed risk for “perimesencephalic SAH” is approximately same asfor general population
Intracranial Aneurysms
Epidemiology
• prevalence 1-4% (20-30% have multiple)
• 1
;
>M; 35-65 yr (mean age of presentation is 50 yr)
Types
• saccular (berry)
most common type
located at branch points of major cerebral arteries (circle of Willis)
85-95% in carotid (anterior) system, 5-15% in vertebrobasilar (posterior) circulation
• fusiform
atherosclerotic
more common in vertebrobasilarsystem, rarely rupture
• infectious(mycotic)
secondary to any infection of vessel wall, 20% multiple
60% Streptococcus and Staphylococcus
• 3-15% of patients with bacterial endocarditis
Most Common Locations of Saccular
Aneurysms
• Anterior communicating artery
(ACom):30%
• Posterior communicating artery
(PCom):25%
- MCA:20%
• Basilar tip:7%
Risk Factors for Saccular Aneurysms
Smok ing
HTN
Adult Polycystic kidney disease
Ehlers-Danlos syndrome
Family history:>2 first-degree relatives
Risk Factors
• autosomal dominant polycystic kidney disease (15%)
• fibromuscular dysplasia (7-21%)
. AVMs
• connective tissue diseases (Ehlers-Danlos syndrome, Marfan syndrome)
• family history
• bacterial endocarditis
• Osier-Weber-Kendu syndrome (hereditary hemorrhagic telangiectasia)
• atherosclerosis, HT N, and smoking
• trauma
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Table 16. Five Year Cumulative Rupture Risk in Unruptured Aneurysms Based on Size and
Location
Long-Term.Serial Screening for Intracranial
Aneurysms in Individuals wilti a Family History
d Aneurysmal Subarachnoid Hemorrhage:A
Cohort Study
lance!Neurol 2014:13:385-392
Purpose: Toei amine the y.eld of long-term serial
screening lor Intracranial aneurysms loi Individuals
with a positive famdy history ol aneurysmal
subarachnoid hemorrhage (aSAH) (hroor more first
degree relatives who have had aSAH or unruptured
Intracranial aneurysms).
Study:Screening results Iron April 11993 toApril 1
2013wece reviewed in a cohortstudy.MSAor CIA was
done from ages16-18 to ages 65 )0.Alter a negative
screen, individuals were advised to contact IheOnme
hsSyrfoi follow-up.
Results:Aneurysmswere identified in11% of
indivvduals al (listscreening|n-458),8% at second
screening (n*
261).5% atlhird screening (n-128|.
and &% atfourth screening (n*63|.Smoking (OR 2.
)
.
95% Cl1.2-5 j), history of previous aneurysms(3.9.
1.2-12.
)).and fami al history olaneurysms(3.5.
1.68.1) were significant risk factorsfor aneurysm at
first screening. History ol previous aneurysms vrastte
only significant risk factor for aneurysms at follow -up
screening (HR 4.5.95% Cl1.1-18.)).
Conclusions: Ihe benefit ol long- term screening in
individuals with a family history of aSAH issubstantial
up to and after 10 yr of follow-up and twn initial
negative screens.
Cavernous Carotid ACAorACom/MCA/ICA Vertebrobasilar/PCAtPCom
*7mm 0% 0% 2.5%
7-12 mm 0% 2.6% 14.5%
13-24 mm 3%
v
24 mm
14.5% 18.4%
6.4% 40% 50%
ACA = anterior cerebral artery:ACom = anterior communicating artery:ICA -internal carotid artery:MCA - middle cerebral artery: RCA- posterior
cerebral artery: PCom = posterior commuiicating artery.
Table adopted Irorn the ISUIA Trial: lancet 2003:362:W3-!10
Clinical Features
• rupture (90%), most often SAH, but 30% ICH, 20% IVH, 3% subdural bleed
• sentinel hemorrhage (“thunderclap H /A") > requires urgent clipping/coiling to prevent catastrophic
bleed
• mass effect (giant aneurysms)
• ICA or ACom aneurysm may compress:
the pituitary stalk or hypothalamus causing hypopituitarism
the optic nerve or chiasm producing a visual field defect
basilar artery aneurysm may compress midbrain, pons (limb weakness),or CN III
PCom aneurysm may produce CN III palsy
intracavernous aneurysms (CN 111, IV, VI, V2, VI)
• distal embolization (e.g. amaurosisfugax)
• seizures
• H/A (without hemorrhage)
• incidental CT or angiography finding (asymptomatic)
Investigations
• CTA, MRA, cerebral angiogram
Treatment
• ruptured aneurysms
overall trend towards better outcome with early surgery or coiling (48-96 h after SAH)
treatment options: surgical placement of dip across aneurysm neck, trapping (clipping of
proximal and distal vessels), coiling using (iuglielmi detachable coils, (low diversion stents,
wrapping (last resort)
choice of surgery vs. coiling: consider location,size,shape, and tortuosity of the aneurysm,
patient comorbidities, age, and neurological condition; in general:
endovascular coiling > clipping for ruptured intracranial aneurysmssuitable for both
treatments -> greater survival benefit at 1 yr with sustained effect for up to 7 yr post-treatment
coiling: posterior > anterior circulation, deep/eloquent location, basilar artery bifurcation/
apex, older age, presence of comorbidities, presence of vasospasm
clipping:difficult endovascular access, broad aneurysmal base, branching arteries at the
aneurysm base, tortuosity/atherosclerosis of afferent vessels, dissection, hematoma, acute
brainstem compression
• unruptured aneurysms
average 1.4% annual risk of rupture; predictors include: age, HTN, history of SAH, aneurysm size
and location, and geographical region (Finnish people = 3.6 times increased risk;Japanese people
= 2.8 times increased risk)
no clear evidence on when to operate; need to weigh life expectancy
• risk of niorbidity/mortality of SAH (20-50%) vs. risk of coiling (
-2%)
generally treat unruptureu aneurysms >10 mm
• treatment guided by balance of risks of SAH per ISUIA and PHASES and of intervention per
centre experience and outcomes
follow smaller aneurysms with serial angiography
The Unruptureil Intracranial Aneurysm Treatment
Score
Ffc.rc ogy 2015:85(101:881 839
Purpose: To develop an unruptured intracranial
aneurysm (UIA) treatmentscore|UIA!$|model lira!
includes and quantifies key lectorsinvolved in clinical
decision- making m the management of UlAs and lo
assess agreement for this model airo'g specialists in
UIA management and research.
Methods: An international mullidisup inary
(neurosurgery, neuroradiology. neurology, clinical
eptdeminlogyl group of 69 specaiists was convened
to develop and validate the UIAIS model using a
Delphi consensus method .
Results: Hie UIAIS accountslor 29 key factors m UIA
management.
Conclusions: T'
is novel UIA decs on guidance
study captures an encellent consensus among
highly informed individuals on UIA management,
irrespective of their underlying specialty.
See landmark Neurosurgery Trials ta£>le for more
information on the natural history ol unrupluied
intracranial aneurysms and the risk associated with
the repair.
Intracerebral Hemorrhage
Definition
• hemorrhage svithin brain parenchyma, accountsfor ~10% of strokes
• can dissect into ventricular system (IVH) or through cortical surface (SAH )
Etiology
• HT N (usually causes bleeds at putamen, thalamus, pons, and cerebellum)
• hemorrhagic transformation (reperfusion post-stroke,surgery,strenuous exercise, etc.)
• vascular anomalies
aneurysm, AVMs, and other vascular malformations (see Vascular Malformations, NS27)
venoussinus thrombosis
arteriopathies (cerebral amyloid angiopathy, lipohvalinosis, vasculitis)
location of ICH
• Basal ganglia/internal capsule (50%)
• Thalamus (15%)
• Cerebral white matter (15%)
• Cerebellum/brainstem - usually
pons (15%)
• Other (5%)
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NS26 Neurosurgery Toronto Notes 2023
• tumours(1%):often malignant (e.g. GBM, lymphoma, metastases)
• drugs(amphetamines,cocaine, alcohol, anticoagulants, etc.)
• coagulopathy (iatrogenic,leukemia, thrombotic thrombocytopenic purpura, aplastic anemia)
• CNS infections(fungal,granulomas, herpessimplex encephalitis)
• post-trauma (immediate or delayed,frontal and temporal lobes most commonly injured via coupcontrecoup mechanism)
• eclampsia
• postoperative ( post-carotid endarterectomy cerebral reperfusion, craniotomy)
• idiopathic
ICH Score Components
• GCS score (3-4-2 pts;5-12-1pt,
13-15-
0pt)
. ICH volume(>30 cm~
1pt,<30 cm-Q
pi)
. Presence of IVH (yes-1pt no-0 pt)
. Infratentorial origin (yes-1pt,no'
0
• Age (i80-1pt <80 *
0 pt)
Epidemiology
• 12-31 cases in 100000 population per yr
Surgical Dedsrca Makiag inBrain Hemorrhage:
Hew Analysis of theSIKH.STICK IIand STITCH
(Tranra) Bandocaed Trials
Stroke 2015:50:1108-1115
Summary:IheSICH(Snrgical Trial in Lobar
IntracerebralBesonhage)I(“1033 patients)and
II(n401patents)trials randomized patients with
spontaneoss ateceehralhemorrhage (ICH)to
early sargeryorrmtaltyaiasenatrire treatment.The
STITCH (Tranma)triadimestgatedthese options in
the entailof tead-apredpatents(n-170 patients).
Ilea-analyse of spontaneous ICH patients suggests
that thosepresentrgnoa 6CS0110-13 anda large
KHare more Skety to benefit from early surgery
than'
Josepresentegndh a CCS ontside this range.
S»gical treatseaof fsroatic ICH with CCS10-13
-ares - a- . oe-eSca ariOMS
Refer athe landmark lenrosnrgery trialsable for
details of STICH.
Risk Factors
• increasing age (mainly >55 yr)
• male
• HTN
. Black/Asian > White
• previous cerebrovascular accident of any type (23 times risk)
• both acute and chronic heavy EtOH use; cocaine, amphetamines
• liver disease
• anticoagulants
Clinical Features
• TIA-like symptoms often precede ICH, can localize to site of impending hemorrhage
• gradual onset of symptoms over minutes-hours, usually during activity
• H/A, N/Y,and decreased LOG are common
• specific symptoms/deficits depend on location of ICH
Investigations
• baseline severity score such asthe ICH Score should be performed as part of the initial
workup
• hvperdense blood on non-contrast CT
• CTA routine,ifspot sign (contrast in the hematoma) demonstrated there is high likelihood of clot
growth
Spetder-Martin AVM Grading Scale
Rea Store
Size
Treatment
• patientsshould be transferred to and managed in a neuro-ICC orstroke unit
• medical
• decrease MAP to pre-morbid level or by -20% (target BP 140/90) in emergency department
• check partial thromboplastin time/international normalized ratio (PTT/1NR), and correct
coagulopathy (immediate reversal of anticoagulation)
• control raised ICP (see Intracranial Pressure Dynamics, SS4 )
• corticosteroidsshould NOT be used for elevated ICP in ICH
0-3 re
Wire 2
4c- 3
location
hfrdow*
0
Oogocct
OtepVzoonsOrainagt
Httpceswt
Presetf
I
levetiracetam/phenytoin for seizure prophylaxis
• follow electrolytes (S1ADH common)
• angiogram to rule out vascular lesion unless >45 yr,known HTN,and putamen/thalamic/
posterior fossa ICH (yield -0%)
0
ZVU varies w? ukdntod by nddntg trio 3 individual
Sperite-HortiSafe scare horn the above table.
-9- a 2 cn hnctx e rcr
-etoquetit locaticci without
bawtage = Grade I
• surgical
* craniotomy with evacuation of clot, treatment ofsource of ICH (i.e.AVM, tumour, cavernoma),
ventriculostomy to treat hydrocephalus
• indications
symptoms of raised ICP or mass effect
rapid deterioration (especially ifsigns of brainstem compression)
favourable location (e.g. cerebellar, non-dominant hemisphere)
young patient (<50 yr)
suspected tumour, AVM, aneurysm, or cavernoma (resection or clip to decrease risk of
rebleed)
• contraindications
small bleed:minimal symptoms, GCS >10
poor prognosis: massive hemorrhage (especially dominant lobe), low GCS/coma, lost
brainstem function
medical reasons (e.g.advanced age,severe coagulopathy,difficult location (e.g. basal ganglia,
thalamus)) n
u
Prognosis
• 30 d mortality rate 44%,mostly due to cerebral herniation
• rebleed rate 2-6%,higher if HTN poorly controlled +
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XS27 Neurosurgery Toronto Notes 2023
Vascular Malformations
Types
• AVMs
• cavernous malformations (cavernomas, cavernous hemangiomas/angiomas)
• venous angioma
• capillary telangiectasias
• AY1 (carotid-cavernous fistula, dural AYF,vein of Galen aneurysm)
•
“angiographically occult vascular malformations” (any type, 10% of malformations)
Arteriovenous Malformations, Cavernous Malformations,
and Dural Arteriovenous Fistulas
Table 17. Comparison of Pathoetiology,Clinical Features, and Treatment of Arteriovenous
Malformations, Cavernous Malformations, and Dural Fistulas
Arteriovenous Malformations Cavernous Malformations Dural Fistulas
Definition Tangle of abnormal vessels/arteriovenous Benign vascular hamartoma
shunts,with no intervening capillary beds consisting ol irregular sinusoidal
or brain parenchyma;usually congenital vascular channels located within
Frstu'as connecting dural arteries to
dural veinsor the dural sinus
frequently occur at the transverse and
the brain without intervening neural cavernous sinuses,but can be found at
tissue or associated large arteries/ every cranial dural sinus
Hypothesised to be related to venous
Several genes now described:CCM1. sinus thrombosis formation,and
subsequent microvascular shunt
lor.mat on within the dura between
arteries and veins
Unknown trueincidence
Constitute 10-15% of all intracranial
vascular abnormalities
veins
CCM2.CCM3
Epidemiology Prevalence -0.14%.M:F"2:1.average age Prevalence ol0.10.2%,both
sporadic andhereditary forms
described
Figure 21. MRI of cavernous
malformation
A. T2-weighted imaging MRI
B.Gradient echo sequencing MRI
at diagnosis-33 yr
15-20% ol patients with hereditary
hemorrhagic telangiectasia (Osier-WeberRendu syndrome)will havecerebral AVUs
Clinical Features Hemorrhage (40-60%);small AVMs are
more likely to bleed due to directhigh
pressure AV connections
Seizures (50%);more commonwith
larger AVMs
Mass effect
Focal neurologicalsigns secondary
to ischemia (high (low "steal
phenomena")
localized H/A,increased ICP
Bruit (especially with dural AVMs)
May be asymptomatic (“silent")
Investigations MRI (flow void),MRA
Angiography (7% will also have one or
more associatedaneurysms)
Seizures (60%),progressive
neurological deficit (50%),
hemorrhage (20%),H/A
Often an incidental finding
Hemorrhage risk less than AVM.
usually minor bleeds
Asymptomatic,pulsatile tinnitus if
involving sigmoid or transverse sinuses,
bruits.H/A
Carotid cavernousinvolvement
classically produces proptosis,
chemosis.and bruits
Symptoms of SAH,S0H.or ICH
Clinical Course ofUntreated Cerebral Cavernous
Nalforwations (CCM)
laxe:leant2015 pi.
^
1474-4422(15)00303-8
Purpose. loohCam precise estimates and predictors
of tteris< of rtratrana semorrhage (ICH) in patients
urth.
^
treated cerebral cavernous malformations
(CCMs).
Methods Colected individual patient data from
iwestigMhtsof pubkstedstudies on MEDLINE aid
Eriasesnce mteoSon cut April 201517 cohorts
from 6 sides.-16211) on clmcalcourse from CCM
dagnpss 5rsiCCM treatment or last armlaile
Hnp
Results:2Mof tte1520patients experienced ICH
darng 5187persoc-yr -nllouv-up (Kaplan-Meier
estoaSd5 yr risk 15.8%.95% Cl13.7-17.9).ICH
irtnSyr of CCM degnoss was associated with
clinical presernateo with ICH or focal neurological
deScitw-thoatbra n imaging evidenceof recent
renrrtage(is.Oder presentations;HR 5,6.95% Cl
32-9.7)asd»8b-amstem CCM location|vs.other
locahoos;Hi44.95% 02.3-8.6).
Conclusions :liMode of deucal presentation and
(2) CCM scatoc a-e rdeoendentlyassocratedwith
ICH w“
- 5 yr of CCM diagnosis. The risk of recurrent
hemortage‘
-or a CCM is greater than the risk of the
hrst ere:rddec!res over 5 yr.
T2-weighted image MRI|nonenhancing)
Gradient echo sequencing (best for
diagnosis)
Surgical excision:
Only appropriate for symptomatic
lesions that are surgically
accessible (supratentorial lesions
are less likely to bleed than
infratentorial lesions)
Ang ogr aphy remains the gold standard
Non-enhanced CT to rule out hemorrhage
MRI:however,this does not demonstrate
the arterial supply to the fistula
Approach is dependent on size,location
and symptoms,and includes:
Conservative treatment
Neuroradiotogical endovascular
interventions
Radiation therapy
Surgery
Combination olthe above
Decreases risk of future hemorrhage
and seizure
Surgical excisionis treatment of choice
even in Spetzler-Martin gradesI-IIwith
general good health
SRS is preferred tor small (<3 cm) or very
deep lesions
Endovascular embolization (glue,balloon)
can be curative (5%) or used as adjuvant
to surgery or SRS in larger lesions
Conservative (e.g. palliative
embolization,seizure control if
necessary)
12-66% mortality.23-40% morbidity
(serious neurologicaldeficit) per bleed
Risk olmajor bleed in untreatedAYMs;
2-4%/yr
Outcomes dependon Speltzer-Martm
grade
Treatment
Annual bleeding rates:0.25-1.1% for 8.1% anrnalrisk of hemorrhage
supratentorial,2-3% for brainstem 6.9% annual risk for non-hemorrhagic
Symptomatic lesions have a higher neurological deficit
hemorrhage risk than asymptomatic 10.4%mortality rate
Outcomes influencedby dural fistula
type (presence olcortical venous
drainage -•poorer outcomes)
Prognosis
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Cerebrospinal Fluid Fistulas
Suspect CSF fistula in patients with
otorrhea or rhinorrhea after head trauma
or recurrent meningitis
Etiology
• cranial orspinal
• traumatic:after head trauma,iatrogenic (post-transsphenoidal surgery, post skull base surgery)
• nontraumatic:high pressure (hydrocephalus, tumour), normal pressure (bone erosion secondary to
infection, congenital defect)
Clinical Features
• otorrhea or rhinorrhea (clear fluid)
• low pressure H/A (worse when sitting up)
• confirmatory testing for CSF:(5-transferrin test, quantitative glucose analysis of fluid, “ring sign",
“reservoir sign'
Investigations
• CT (detect pneumocephalus,fractures,skull base defects), water contrast CT cisternography
Ring Sign:If CSF is mixed with blood.
Allow CSF to drain onto the surrounding
sheets;positive if dear in centre with
surrounding blood coloured ring (double
ring sign)
Reservoir Sign:Gush of CSF leaks out in
certain head positions (i.e.teapot sign):
not specific or sensitive
Treatment
• lower ICP (avoid straining, acetazolamidc to reduce CSF production, modest fluid restriction)
• persistent leak: may require continuous lumbar drainage via percutaneous catheter
• surgical indications: traumatic leak lasting >2 wk,spontaneous leaks,delayed onset of leak after
trauma orsurgery, leaks complicated by meningitis
Red Flags for Back fein
BACK PAIN
Bowel/Bladder (retention or
incontinence)
Anesthesia (saddle)
Constitutional symptoms
“K"hronic disease
Parasthesia
Age >50 or <20
IV drug use
Neuromotor deficits
EXTRACRANIAL PATHOLOGY
Approach to Limb/Back Pain Cauda Equina
Urinary retention or incontinence,fecal
incontinence or loss of anal sphincter
tone,saddle anesthesia,uni/bilateral leg
weakness/pain
Malignancy
Age >50,previous Hx of cancer,pain
unrelieved by bed rest constitutional
symptoms
Infection
Increased ESR.IV drug use.
immunosuppressed.fever
Compression Fracture
Age >50,trauma,prolonged steroid use
• see Orthopaedic Surgery
Extradural Lesions
Post circulation
Ant circulation
AXIAL SECTION OF
THORACIC SPINE
-
[
Dorsal
funiculus
asciculus gracilis
.Fasciculus cuneatus Posterior spinal
artery
Dorsal horn
(sensory!
.lateral
corticospinal
Lateral hon tract (efferent)
(autonomic! j 'jL
*onlv present
T1-LZS2 SS \
-
lateral
funiculus
,O J
n .f
-Spinothalamic
tract (afforcntl Ventral horn
(motor)
Anterior
spinal artery
Ventral
funiculus Anterior
corticospinal
tract (efferent)
Posterior spinal aa.
Anterior
segmental
medullary a.
Arachnoid mater /.Dura mater
Post & ant. interior spinal a.
reticular aa.
Branch to vertebral
body & dura mater
Dorsal branch - of intercostal a
Spinal a.
Thoracic aorta
r1
L J
Intercostal a. © Natalie Cormier 2D1S.after Takami lijima +
Figure 22. Vascular supply of spinal cord
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Root Compression
Sensory Fibres
• Fasciculus gracilis/cuneatus:
proprioception,fine touch,vibration
• Spinothalamic tract: pain and
temperature
Motor Fibres
• Corticospinal tract:skilled
movements
•radiculopathy is a pain and/or sensorimotor deficitsyndrome that involves compression of a nerve
root.Nerve compression generally occurs as a result of disc herniation, degenerative disc diseases
(spondylosis),instability, and masses (rare)
•patients generally present with referred pain,sensory changes (numbness and/or tingling) or
weakness. Whereas patients might sometimes describe sensory changes in a dermatomal distribution,
the referred pain will not be in a dermatomal distribution.The areas of pain and altered sensorium
may be incongruent
•muscle innervation hasless overlap than sensory innervation and hence is a better predictor of level of
pathology
Differential Diagnosis
•herniated disc
•neoplasm (neurofibroma,schwannoma)
•synovial cyst,abscess
•hypertrophic bone/spur
Cervical Disc Syndrome
Etiology
• nucleus pulposus herniates through annulus fibrosus and impinges upon nerve root, most commonly
Disc herniations impinge the nerve root
at the level below the interspace fie.
Clinical C5-6disc affectsthe C6 nerve root)
Features
• pain in arm follows nerve root distribution,worse with neck extension,ipsilateral rotation, and lateral
flexion (all compressthe ipsilateral neural foramen)
• LMN signs and symptoms (diminished reflexes,non-spastic motor weakness)
• central cervical disc protrusion may cause myelopathy as well as nerve root deficits
Investigations
• if red flags: cervical spine (C-spine) x-ray,Cl'
, MR1 (imaging of choice)
• only consider HMG/nerve conduction studies if diagnosis uncertain and presenting more as peripheral
nerve issue
Treatment
• nonsurgical
• no bed rest unlesssevere radicular symptoms
• activity modification, patient education (reduce sitting,lifting)
physiotherapy, exercise programsfocus on strengthening core muscles
• analgesics;NSAlDs are more efficacious
• avoid cervical manipulation like traction
• surgical indications
anterior cervical discectomy is the usual approach (posterior foraminotomy with discectomy is
the other option)
• intractable pain despite adequate conservative treatment for >3 mo
progressive neurological deficit
Prognosis
• 95% improve spontaneously in 4-8 wk
Table 18.Lateral Cervical Disc Syndromes
C4-5 C5-6 C6-7 C7-T1
Root Involved C5 C6 C7 C8
Incidence
Sensory
Motor
2% m. 69% 10%
Shoulder
Deltoid,biceps,
supraspinatus
No change
Middle finger
Biceps,wrist extensors Triceps
Thumb Ring finger.Sth finger
Digital flexors,intrinsics
Reflex Biceps,brachioradialis triceps Finger jerk (Hoffmann's
r n
i.J
+
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Degenerative Cervical Myelopathy
Definition
• progressive degenerative process of cervical spine leading to canal stenosis; congenital spinal
stenosis;degeneration of intervertebral discs;hypertrophy of dura or ligaments;subluxation; altered
mobility; telescoping of the spine due to loss of height of vertebral bodies; alteration of normal lordotic
curvature
• resultantsyndromes:mechanical neck pain,radiculopathy (root compression),myelopathy (spinal
cord compression)
Epidemiology
• typically begins at age 40-50,M>F,most commonly at the C5-C6 > C6-C7 levels
Pathogenesis
• any of:disc degeneration/herniation,osteophyte formation, ossification, and hypertrophy of
ligaments
• pathophysiology includesstatic compression,dynamic compression, and vascular compromise
Clinical Features
• insidious onset of mechanical neck pain exacerbated by excess vertebral motion (particularly rotation
and lateral bending with a vertical compressive force Spurling'
stest)
• the earliest symptoms are gait disturbance and lower extremity weakness or stiffness
• occipital H/A is common
• radiculopathy may involve 1 or more roots,and symptomsinclude neck,shoulder, and arm pain;
paresthesias;and numbness
• cervical spondylotic myelopathy may present with:
weakness (upper > lower extremity),lower extremity weakness (corticospinal tracts) is most
worrisome complaint
decreased dexterity,lossof fine motor control
sensor)'changes
UMN findings such as hyperreflexia,clonus, and Babinski reflex
funicular pain,characterized by burning and stinging ± Lhermitte’
ssign (lightning-like
sensation down the back with neck flexion)
Investigations
• x-ray of cervicalspine ± flexion/extension (alignment,fractures)
• MR1 most usefulfor determination of compression of the neural element
• CT is only used for better determination of bony anatomy (i.e.OPLL)
• HMG/nerve conduction studiesreserved for peripheral nerve investigation
Cervical spondylotic myelopathy isthe
most common cause of spinal cord
impairment
'
Clinical Grading Scoresto Assess CSM
• Modified Japanese Orthopaedic
Association (mJOA)
• Nunck Grade
• Neck Disability Index
A ClinicalPractice Gnidetine for dtMaaagcntn:
ofPrintsnritk DagncratinCtmul
Mjelopatbj(OCM):iKoaandrionsta
Patients with Mild. Moderate,aadSeme Disease
and NonaayelcpatAic Patients witkEvidence of
CordCoapressioo
(<obil Spue Josraa!20W:7|3S)2«S43S
Sente ndaoderateDCM Moderateendeete
soggestnag stoegrecosneodatoo of sorgcal
initriwtioa.
Mild DCM:legIontoIonerdetce saggssti-g
offeringsorgcalicteneitiOfl or a sinefared
retrain!trio:aaddeoo-ogerriienasageaeot
naitiaMy persaed.coasder operatneEotenertoo if
endeset of oenrologcai deteriocatoa_
oo-nyelopatkk patientsnitkoitradialopatky
In sadpriestsnidisagagendeace af cemcai
popAjIacticsBrgerj:coaaeledacate.and felon
cfaolp.
an-nyelopatkic patientsvitk radiolopatky:
Sock prietSsnttcsgcgerdetceof terrcal
cord canpressioo are at a tgter risk of deielopng
•rjekipadjaadskatid becaarseled.OMersurgical
or nosoperetiae treatamt nrfl appraprratsfo5ow-«p
and stiict_red reatiitatioe.
Figure 23.CT (left) and MRI (right)representations of cervical spondylosis
Images courtesy of Or.Eric Masskotte r n
L J
Treatment
•nonsurgical: physiotherapy, anti-inflammatory medications
•surgical:anterior approach (anterior cervical discectomy or corpectomy), posterior approach
(decompressive cervical laminectomy)
•in multilevel degenerative cervical myelopathy (DCM), both anterior and posterior options are
acceptable approaches with generally comparable outcomes
• with kyphosis -> anterior approach generally preferred
+
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• with preserved cervical lordosis -> posterior approach generally preferred
• surgical indications: myelopathy with motor impairment, progressive neurologic impairment,
intractable pain
• complete remission almost never occurs;surgical decompression stops progression of disease in
almost all cases; 80'V, of patients experience neurological improvement
Table 19.2017 Summary AO Spine-CSRS Guideline for the Management of Degenerative Cervical
Myelopathy
Patient Population Level of Recommendation Guideline/Recommendation
Severe DCM (raJOA 0-H)
Moderate 0CM|mJ0A 1244)
Mild DCM {mJ0A1S.1T)
Strong
Strong
Surgical intervention isrecommended
Surgical intervention is recommended
Surgical intervention or structured rehabilitationis recommended:
consider surgery if withneurologic deterioration or failure to
improve
Prophylactic surgery isnot recommended
Weak
Non-myelopathic patients with Weak
cord compression and without
radiculopathy
Non-myElopathic patients with cord Weak
compression and withrad.allopathy
Either surgical intervention or nonoperative treatment(dose
follow-up or structured rehabilitation)
Lumbar Disc Syndrome
Definition
• compression of nerve roots caused by herniation of the nucleus pulposus through the annulus fibrosus
of an intervertebral disc in the lumbar spine
Etiology
• posterolaterally herniated disc compressed nerve root exiting BELOW the level of the disc or the
traversing nerve root
• far lateral disc herniation compressed nerve root AT the level of the disc or the exiting nerve root
• central herniation may cause cauda equina compression or lumbar stenosis (neurogenic claudication)
Clinical Features
• initially back pain,then leg pain > back pain
• limited back movement (especially forward flexion) due to pain
• motor weakness, dermatomal sensory changes, decreased reflexes
• exacerbation with Valsalva; relief with flexing the knee or thigh
• nerve root tension signs
• straight leg raise (SLR) (Lasegue’s test) or crossed SLR (pain should occur at less than 60°)
suggests L5, SI root involvement
• femoral stretch test suggests L2, L3, or L4 root involvement
Figure 24.T2-weighted MRI of
lumbar disc herniation
Investigations
• MRI is modality of choice
• x-ray spine (only to rule out other lesions), CT (bony anatomy)
myelogram and post-myelogram CT (only if MRI is contraindicated)
See landmark Heu-osa-gery Inals table for mote
i-brmat^
"e SPOBI trial fir outcomes of surgery
*
.rorooeraive care foe lumbar diseberniabun.
Treatment
• nonsurgical (same as cervical disc disease)
• surgical indications:same as cervical disc and cauda equina syndrome
Magnetic BesoiaiceImaging inFollow-Up
Assessaeniof Sciatica
IBM 2013:3S85$9-M)0?
Backgroud: Fo cn .:MB) is a coistroveisia!
etkod for nKSrrgsciatica c patients wifi known
liBSar-dsckertateo.
Metlods: Paridpants(n-283|weierecruited
froa a s
=ul2:eoas. parallel,raodomraed study
coaparmg surgery aid conservative care loi sciatica
(aeSciatica trial).MBI and clinical assessment weie
usderulei prMreatmett and 1 yi post-tieatment
’ri:~ to nsualiae disc herniation and
evaluate outome.
Besitts 1p.4sc tar- ation was visible in 35%
wis a fanuraieoutcome (complete,or nearly
carpea sy-jtom resolntjos) acid m 33% wifi
ai uifavou-cSie aut:ire (NI.70).A favourable
outcome was-eocried v:85%. of patients with disc
henetoa erd13% wiiewt isc heiniatioo (H)J0|.
Conclusions:Aretoniccl abnormalities visible on
itbeSrd1011 perne-treatmentforsciabca due to
taber-dsc temaSoo cou d not distinguish patients
witt resobtoa of theirsymptomsfrom patientsstill
eipe-ercog symptoms.
Prognosis
• 95% improve spontaneously within 4-8 wTk
• those who do not improve writh conservative treatment achieve symptom relief quicker with surgery
than continuation of conservative management; however, the long-term outcome after surgery is
comparable to conservative therapy
• do not follow patients with serial MRIs; clinicalstatusis more important at guiding management
Table 20. Lateral Lumbar Disc Syndromes
13-4 L4-5 L5-S1
Root Involved L4 L5 S1
r -\
Incidence <10%
Femoral pattern
Medial leg
45% 45% i
_ j
Pain Sciatic pattern
Dorsal foot to hallux
Lateralleg
Extensor halloas longus (hallux
extension)
Medial hamstrings
Sciatic pattern
Sensory Lateral loot
tibialis anterior (dorsiflexion) Gastrocnemius,soleus (plantar +
flexion)
Achilles
Motor
Reflex Patellar
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Table 21.Differentiating Conus Medullaris Syndrome from Cauda Equina Syndrome
Conus Medullaris Syndrome Cauda Equina Syndrome
Onset
Spontaneous Pain
Gradual, unilateral
Rare,if present usually bilateral,symmetric in Severe, radicular type:in perineum, thighs,
perineum or thighs
Saddle:bilateral and symmetric:sensory
dissociation
Sudden,bilateral
legs. back,or bladder
Sensory Deficit Saddle:no sensory dissociation:may be
unilateral and asymmetric
Symmetric:paresisless marked:fascicutabons Asymmetric:paresis more marked: atrophy
may be present:fasciculations rare
Motor Deficit
may be present
Reflexes Only ankle jerkabsent (preserved knee jerk) Knee and ankle jerk may be absent
Sphincter dysfunction presents late; impotence
lessfrequent
Autonomic Symptoms (bladder dysfunction. Urinary retention and atonic anal sphincter
impotence.etc.) prominent early:impotence frequent
Cauda Equina Syndrome
Etiology
• compression or irritation of lumbosacral nerve roots below conus medullaris(below L2 level)
• decreased space in the vertebral canal below L2
• common causes:herniated disc ± spinal stenosis,vertebral fracture, and tumour
Causes of Cauda Equina Syndrome
• Lumbar disc herniation
• Spinal stenosis
. Spinal tumour
• Epidural abscess
• Hematoma
• Trauma
Clinical Features
• usually acute (develops in less than 24 h ); rarely subacute or chronic
• motor (LMN signs)
weakness in multiple root distribution
reduced deep tendon reflexes(knee or ankle)
• autonomic
» urinary retention (or overflow incontinence) and/or fecal incontinence due to loss of anal
sphincter tone
• sensory'
low back pain radiating to legs (sciatica) aggravated by Valsalva maneuver and by sitting;relieved
by lying down
bilateral sensory loss or pain:depends on the level affected
saddle area (S2-S5) anesthesia
• sexual dysfunction (late finding)
Investigations
• urgent MRI to confirm compression of S2-S3-S4 nerve root by a large disc herniation
• post-void residual very helpful to determine if true retention is present; volumes controversial but
anything over 250 cc in a healthy individual is cause for concern
Treatment
• surgical decompression (<48 h) to preserve bowel,Madder, and sexual function, and/or to prevent
progression to paraplegia
• consult radiation oncology for urgentsymptomatic management if palliative oncology patient
Prognosis
• markedly improves with surgical decompression
• recovery correlates with function at initial presentation:if patient is ambulatory, likely to continue to
be ambulatory;if unable to walk, unlikely to walk aftersurgery
Lumbar Spinal Stenosis
Etiology
• congenital narrowing ofspinal canal combined with degenerative changes(herniated disc,
hypertrophied facet joints, and ligamentum flavum)
Clinical Features
• gradually progressive back and leg pain with standing and walking that is relieved by sitting or lying
down or movementsinvolving lumbar flexion (e.g.riding a bicycle,leaning over a shopping cart);
neurogenic claudication 60% sensitive
• neurologic exam may be normal,including straight leg raise test
See landmark Neurosurgery trials(able lor more
information on the SPORI trial lor outcomes ol
s urgery n. nonoperative care forsymptomatic lumbar
spinalstenosis.
Investigations
• MRI is best to confirm and localize the level ofstenosis(unlike nerve root compression which can be
localized with clinical exam)
L J
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Treatment
• nonsurgical: NSAlDs, analgesia, physical therapy
• surgical:laminectomy with root decompression
• fusion typically advised if evidence of segmental instability prior to surgery (e.g. in flexion/
extension x-rays)
Neurogenic Claudication
Etiology
• ischemia of lumbosacral nerve rootssecondary to vascular compromise and increased demand from
exertion,often associated with lumbar stenosis
Key Features of Neurogenic vs.
Vascular Claudication
• Neurogenic Claudication:
dermatomal distribution with
positional relief occurring over
minutes
• Vascular Claudication:sclcrotomal
distribution with relief occurring with
rest over seconds
Clinical Features
• dermatomal pain/paresthesia/weakness of buttock, hip, thigh, or leg initiated by standing or walking
• slow relief with postural changes (sitting >30 min), NOT simply exertion cessation
• induced by variable degrees of exercise or standing
• may be elicited with lumbar extension, but may not have any other neurological findings, no signs of
vascular compromise (e.g. ulcers, poor capillary refill)
Investigations
• bicycle test may help distinguish NC from vascular claudication (the waist-flexed individuals on the
bicycle with NC can last longer)
Treatment
• same asfor lumbarspinal stenosis
Intradural Intramedullary Lesions
Syringomyelia (Syrinx)
Definition
• cystic cavitation of the spinal cord
• presentation is highly variable, usually progresses over mo to yr
• initially pain, weakness;later atrophy and loss of pain and temperature sensation
Etiology
• 70% are associated with Chiari 1 malformation, 10% with basilar invagination
• post-traumatic
• post-infectious
• post-inflammatory
• tumour
• tethered cord
Clinical Features
• nonspecific features for any intramedullary spinal cord pathology:
initially pain, weakness, atrophy, then loss of pain and temperature (spinothalamic tract) in
upper extremities (central syrinx) with progressive myelopathy over years
sensory loss with preserved touch and proprioception (dorsal column-medial lemniscus
pathway) in a band-like distribution at the level of cervicalsyrinx
dysesthetic pain often occurs in the distribution of the sensory loss
LMN arm/hand weakness or wasting
painless neuropathic arthropathies (Charcot’s joints),especially in the shoulder and neck due to
loss of pain and temperature sensation
Figure 25. T1weighted MRI of
syringomyelia
Investigations
• MRI is best method, myelogram with delayed CT
Treatment
• treat underlying cause (e.g. posterior fossa decompression for Chiari l,surgical removal of tumour if
causing a syrinx)
• rarely doesthe syrinx need to be shunted,
r T
only when progressive and size allows for insertion of tube LJ
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Spinal Cord Syndromes
Complete Spinal Cord Lesion
• bilateral loss of motor/sensory and autonomic function at >4 segments below lesion/injury, with UMN
signs
• about 3% of patients with complete injuries will develop some recovery within 24 h; beyond 24 h, no
distal function will recover
American SpinalInjury Association
Impairment Scale
Grade Descriptiot
A Corpete.oo moton'
sensory below
:e:T3 ogee : level including MS
loarajlete.sensory dot not motor
fcuebe- presented below nearoiogica:
ere ackdmgStS
locoaplete.motor function preserved
seem tesrologiul level,and more
Sax badof Sie key muscles below
nnro'
ogcai level have a muscle
grade <3
laciapfcfe.motor function preserved
oe ow resroiogical level,and more
tor ~af of toe key muscles below
neoroog.Q level bare a muscle
grade >3
Iona!motor aed sensory function
B
Incomplete Spinal Cord Lesion
• any residual function at >4 segments below lesion
• signs include sensory/motor function in lower limbs and “sacral sparing"
(perianal sensation,
voluntary rectal sphincter contraction)
C
Table 22. Comparison Between Incomplete Spinal Cord Lesion Syndromes
Syndrome Etiology Motor Sensory
D
Brown-Sequard Herrisection of cord Ipsilateral LMN weakness at the
lesion
Ipsilateral loss of vibration and
proprioception
Ipsilateral UMN weakness below Contralateral loss of painand
the lesion temperature
Preserved light touch E
Anterior Cord Anterior spinal artery compression Bilateral LMN weakness at the
or occasion
Preserved vibration and
proprioception
Bilateral loss of pain and
temperature
Preserved light touch
lesion
Bilateral UMN weakness below T
2 r
the lesion =
Urinary retention •
1
5
•2 1
Central Cord (most common) Syringomyelia,tumours,spinal 5
I
1 £
tiyperextension injury
Bilateral motor weakness:Upper Variable bilateral suspended
limb weakness (LMN lesion) > sensory loss
Lower limb weakness (UMN lesion) Loss of pain and temperature
Urinary retention
m - N
E
C-
»
proprioception
Bilateral
loss of vibration
loss of vibraboo
and
.
C
proprioception,light touch at and
below the lesion
Preserved pain and temperature
Posterior Cord Posterior spinal artery infarction. Preserved
trauma I
Ifttt Peripheral Nerves
• see Nuurnlogy. N38
Classification
Table 23. Seddon’s Classification of Peripheral Nerve Injury
© Jenna Rebelo 2010y
Nerve Injury Description Recovery
Figure 26.Spinal cord lesion
syndromes Neurapraxia (classI)
Aionotmesis (class It)
Axon structurally intact but fails to function
Axon and myelin sheath disrupted butendoneurium and Spontaneous axonal recovery at1mm/d.max at12 yr
supporting structures intact-» Val erian degeneration
of axon segment distal to injury
Nerve completely transected
Within h to mo (average 6 -8 wkj
Neurotmesis (class III) Need surgicalrepair tor possibility of recovery
Etiology
• ischemia
• nerve entrapment (compression) by nearby anatomic structures, often secondary to localized,
repetitive mechanical trauma with additional vascular injury to nerve
• direct trauma (e.g. transection)
• iatrogenic
Investigations
• clinical exam: muscle bulk and tone, power,sensation, reflexes, localization via Tinel’
ssign
(paresthesias elicited by tapping along the course of a nerve)
• electrophysiological studies: EMG/nerve conduction study (assess nerve integrity and monitoring
recovery after 2-3 wk post-injury)
• labs: blood work (e.g.CBC,TSH , vitamin Bit),CST
• imaging: C-spine, chest/bone x-rays, myelogram, CT, magnetic resonance neurography, angiogram if
vascular damage issuspected
ri
iJ
Treatment
• early neurosurgical consultation if injury issuspected +
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XS35 Neurosurgery Toronto Notes 2023
Table 24. Treatment by Injury Type
Injury Treatment
Nonsurgical: Prevent repeated stress/injur/
,physiotherapy.NSAIDs. local anesthesia/steroid injection
Surgical:Nerve decompression t transposition for progressive deficits, muscle weakness/atrophy, failure of medical
management
Follow up clinically for recovery;exploration if no recovery in 3 mo
If no evidence of recovery, resect damaged segment
Prompt physical therapy and rehabilitation to increase muscle function, maintain joint ROM.maximire return of useful
function
Recovery usually incomplete
Surgicalrepair of nerve sheath unless known to be intact {suture nerve sheaths directly if ends approximate or nerve
graft {usually sural nerve))
Clean laceration:early exploration and repair
Contamination or associated injuries: tag initially with nonabsorbable suture, reapproach within 10 d
Entrapment
Stretch/Contusion
Blood vesselsAxonotmesis
• •
«®rt>
I Neurotmesis 1
I r
Complications
• loss of function (temporarily or permanently)
• neuropathic pain: with neuroma formation
• complex regional pain syndrome: with sympathetic nervous system involvement
Perineurium
Epineurium
/
mmM
Emloneurium SPECIALTY TOPICS
0
•
-
'
Tty Ay
Fascicle
Myelin
Neurotrauma sheath
Trauma Management
• see Emergency Medicine, EU7
Indications for Intubation in Trauma
1 . depressed or decreasing loss of consciousness ( patient cannot protect airway): usually GCS £8
2. need for hyperventilation
3.severe maxillofacial trauma: patency of airway is doubtful
•I. need for pharmacologic paralysis for evaluation or management
• if basal skull fracture suspected, avoid nasotracheal intubation as may inadvertently enter brain
note: intubation prevents patient'
s ability to verbalize for determining GCS
/
Axon -
2
Schwann cell
S1
r,
5
r
I
G
Schwann cell
nucleus
Trauma Assessment
Figure 27. Peripheral nerve structure Initial Management
ABCs of Trauma Management
• see Emergency Medicine, ER2
NEUROLOGICAL ASSESSMENT Glasgow Coma Scale
Eye Verbal
Response Response
Motor
Mini-History
• period of loss of consciousness, post-traumatic amnesia, loss of bowel/bladder control, loss of
sensation, weakness, type of injury/accident
• in urgent situations, remember "SAMPLE-1
'”: signs/symptoms, allergies, medications, past medical
history, last meal, events leading up to the trauma, and baseline functioning
Neurological Exam
• ABCs
• vital signs
- GCS
• brainstem reflexes (if appropriate)
• cranial nerve exam
• motor and sensory exam,including peripheral reflexes
• spine (pain/tenderness, palpable deformity)
• sphincter tone and saddle sensation
• record and repeat neurological exam at regular intervals, as appropriate
Response
4 spontaneous 5 oriented 6 obeys
commands
3 opens eyes 4 contused Slocalizes to
toMice
2 opens eyes 3 inappropriate
to pain wards
Inoeye
opening sounds
pain
4 withdraws
from pan
2 incomprehensible 3 flexion
to pain
(decorticate
postnnng)
1no response 2 extension
to pain
(decerebrate
postering)
Iintubated 1no r-i
response L J
Best response for each component recorded
individually (e
_ g_ E3V3M5)
e13b mild injury:9-T2 is moderate injury;sSis
severe injury
+
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