Neurological Flashcards
What Is Myasthenia Gravis?
Myasthenia gravis (MG) is an autoimmune disorder affect-
ing the postsynaptic membrane of the neuromuscular junc-
tion of skeletal muscle. Autoantibodies against the α-subunit
of the nicotinic acetylcholine receptor nAChR (muscle type
only) cause receptor destruction and transmission failure,
resulting in skeletal muscle weakness and fatiguability. The
nAChR of the autonomic and central nervous systems are
spared.
The incidence of MG varies between 0.25 and 2 per
100,000 with increasing frequency among those older than
60 years. Women are more likely to be diagnosed in the
30–40-year-old age group, whereas men are more often
diagnosed from 60 years onwards [1].
What Is Seronegative Myasthenia Gravis?
Patients who have undetectable levels of antibodies against
nAChR are said to be seronegative. Ten percent of all MG
patients are seronegative. These patients may have nAChR
antibodies that are not detected because of insufficient test
sensitivity [2].
What Are MuSK Antibodies?
○ In a subset of MG patients without nAChR antibodies, muscle-specific tyrosine kinease (MuSK) antibodies are detected.
○ MuSK plays a crucial role in post-synaptic differentiation and clustering of nAChRs at the neuromuscular junction.
○Patients with MuSK MG are predominantly women with prominent oculobulbar weakness and dysarthria.
○ Patients with MuSK antibodies may be resistant to treatment with anticholinesterases
How Does MG Present?
○ Early symptoms are oculobulbar and include fluctuating weakness and fatiguability of the ocular muscles and muscles supplied by the lower cranial nerves (VII-XII).
○ Ophthalmoparesis, diplopia, and ptosis occur in 50% of patients.
○ Dysarthria and dysphagia follow in 15% of patients.
○ These may present with slurred nasal speech or may complain of a choking sensation, and pose an aspiration risk [5].
○ This is followed by generalized disease with fatigue spreading to the upper limbs and hands. The lower limbs tend to be less affected. Wheelchair use due to weakness is uncommon.
○ Symptoms typically worsen at the end of the day, with heat, surgery, and emotional stress.
How Is MG Diagnosed?
History and physical examination are central to diagno-
sis, especially examination of the cranial nerves. Ptosis
upon sustained upward gaze is a characteristic finding.
2. Antibody testing is performed routinely. Antibodies
against nAChR and MuSK are both specific and sensitive
for the detection of MG.
3. The Tensilon test was used in the past to confirm diagno-
sis. Edrophonium chloride was administered intrave-
nously – a short-lived (10 min) improvement confirmed
the diagnosis [6]. It has been replaced by antibody testing
and is largely of historical interest.
4. Neurophysiology. Routine neurophysiological testing
usually yields normal results. Specific testing includes the
following:
• Repetitive nerve stimulation, which has low sensitivity
(70%) for the diagnosis of MG and can be even lower
if disease is limited to the ocular muscles alone [7]
• Single fiber electromyography, which has increased
sensitivity of up to 100% but is not specific and is
greatly operator dependent [8, 9]
What Conditions Are Associated with MG?
MG can be associated with other autoimmune conditions:
• Hyperthyroidism
• Pernicious anemia
• Polymyositis
• Rheumatoid arthritis
• Sarcoidosis
• Sjogren syndrome
• Systemic lupus erythematosus
• Ulcerative colitis
• Therapy with interferons, D-penicillamine, and bone
marrow transplantation can also cause MG [10]
What Is the Role of the Thymus in the Pathogenesis of Myasthenia Gravis?
○ About 75% of patients with MG have abnormal histopathology of the thymus.
- Of these, 85% have thymic hyperplasia and 15% have thymoma.
○ Thymectomy aids symptom control and plays a preventative role in rate and severity of attacks in patients with and without thymoma.
How Is Disease Severity in MG Graded?
A number of disease progression and severity scores can be
utilized, e.g., Manual Muscle Testing (MMT) (Fig. 32.2), the
modified Osserman and Genkins classification (Table 32.1)
and Quantitative Myasthenia Gravis (QMG) scoring may be
used in the preoperative period to establish a baseline [14, 15].
How is MG Treated?
- Symptomatic treatment is with anticholinesterase agents,
e.g., pyridostigmine. Most patients are on a combination
of short-acting and slow-release agents. An intravenous
formulation is available with the following conversion
ratio: 1 mg IV = 30 mg PO. - Immunosuppressive therapy with steroids is used when
pyridostigmine alone does not control symptoms.
Azathioprine is the most commonly prescribed steroid-
sparing agent. It is frequently prescribed in addition to
prednisone because the combination results in greater
efficacy with fewer complications than prednisone mono-
therapy [2]. Patients on long-term steroid treatment are at risk of hypothalamic-pituitary axis suppression. Surgical
stress dosing is discussed in detail in Chap. 19. Patients
taking any dose of glucocorticoid for less than 3 weeks, or
those taking prednisone 5 mg daily for any period of time
are not candidates for stress dosing [17]. - Rapid, immunomodulating treatments, e.g., plasmapher-
esis and intravenous immunoglobulin (IVIG) may be
required for acute exacerbations. Plasmapheresis or
plasma exchange acts by removing circulating anti-AChR
antibodies and immune complexes. It is used to treat
myasthenic crisis or to optimize the unstable myasthenic
patient prior to surgery. It brings about a quick improve-
ment in symptoms (1–7 days), but the effect does not last
beyond 2 months. Plasmapheresis has been described in
patients who are Jehovah’s Witness followers. In these
cases, albumin has been used in place of plasma [18].
IVIG is pooled from thousands of donors. The therapeutic
mechanism is unclear. It has a similar onset, offset, and
efficacy as plasmapheresis [19]. Its use is determined by
availability and familiarity. - Thymectomy is indicated for patients with thymoma and
those with non-thymomatous generalized MG. It
improves symptoms and reduces the requirement for
immunosuppressant therapy and the complications
related to it. It can also be considered in patients with
seronegative MG who have failed to respond to standard
treatment or are treatment intolerant [20].
What Is a Myasthenic Crisis?
○ A myasthenic crisis is a potentially fatal condition due to the rapid deterioration of neuromuscular function.
- It is associated with respiratory compromise due to ventilatory muscle insufficiency and/or weakness of the upper airway muscles.
○ Myasthenic crisis may occur at least once in the lifetime of up to 20% of patients with generalized MG
○ Myasthenic crisis can be triggered by infection, emotional or physical stress, medication changes (especially tapering of immunosuppression), and electrolyte disturbances.
- It can be helpful to perform risk stratification pre-operatively and to discuss the risk of myasthenic crisis with the patient.
○ The Modified Osserman and Genkins classification can be used for risk assessment (Table 32.1) [21, 22].
○ In addition to the foregoing, a pyridostigmine dose >750 mg/day has been associated with increased likelihood of myasthenic crisis [23].
○ Extubation may be delayed if weakness persists at the end of surgery, and the patient may need to be transferred to ICU for ventilation.
○ Plasmapheresis or IVIG treatment may be required.
What Measures Can Be Taken Preoperatively to Ensure That the Patient with MG Is Optimized for Anesthesia and Surgery?
- Pulmonary function tests should be performed to deter-
mine a baseline, to establish criteria for extubation, and to
determine the need for postoperative ventilation. - Liaise with the treating neurologist in the unstable or non-
responding patient for consideration of more complex
preoperative therapies, e.g., intravenous immunoglobulin,
plasma exchange, or pulse steroid therapy [24]. - Plan for postoperative disposition, e.g., ICU referral.
- Assess aspiration risk of patients with dysphagia who
may need further evaluation with video fluoroscopic
assessment. This may help to establish the need for rapid
sequence induction.
What Recommendations Regarding Preoperative Management of MG Medications Should Be Provided to the Patient?
- Continue anticholinesterases, including on the morning of surgery, to avoid preoperative respiratory/bulbar symptoms [25].
- Long-term immunosuppressants can be withheld on the day of surgery, e.g., azathioprine, but the normal steroid dose must be taken if the patient is on a regular glucocorticoid regimen.
What Is the Optimal Time for Elective
Surgery?
Elective procedures should be performed during a period of
myasthenic stability. The patient should be taking the lowest
possible dose of steroid that maintains symptom control.
Surgery should be scheduled early in the day when muscle
strength is better.
The Patient with MG Wants to Know If She Can Have an Epidural for Postoperative Analgesia.
What Do You Tell Her?
○ Neuraxial anesthesia may reduce and even eliminate the need for muscle relaxants for abdominal surgery in MG patients.
○ Epidural analgesia has been used successfully for laparotomy, as a sole anesthetic for laparoscopic cholecystectomy, and even for thymectomy.
○ Case reports are emerging of its safe use for a multitude of indications,
including in obstetric patients [28].
○ Epidural analgesia needs to be carefully titrated.
- A high epidural may compromise respiratory function by affecting intercostal muscle function, decrease forced vital capacity (FVC), and (forced expiratory volume) FEV1, and may necessitate mechanical ventilation.
- In addition, high volume local anesthetic may decrease the sensitivity of the post-junctional membrane to acetylcholine.
○ Ester local anesthetics should be avoided, as anticholinesterases may impair their hydrolysis.
○ Spinal anesthesia has been successfully used for emergency laparotomy, inguinal hernia repair, and transurethral ureterolithotripsy procedures.
Preoperative pulmonary function tests showed reduced
vital capacity (VC), total lung capacity (TLC), and residual volume (RV). In patients with MG, VC is reduced because of
inspiratory and expiratory muscle weakness. Spirometry in
MG patients typically shows a restrictive ventilatory defect
with reasonably well-preserved forced expiratory flow rates.
Patients with restrictive lung disease tend towards propor-
tional reduction in FEV1 and FVC with a normal or increased
FEV1/FVC. The severity of this patient’s PFT abnormality is
mild when categorized according to the American Thoracic
Society Grades for Severity of a Pulmonary Function Test
(Table 32.2) [33, 34].
The patient was a Modified Osserman and Genkins class IIb,
which placed her at increased for myasthenic crisis and aspira-
tion. She was asked to take her pyridostigmine slow release as
usual on the night before surgery and to take her normal dose of
immediate release pyridostigmine on the morning of surgery.
She held the azathioprine but was instructed to take her predni-
sone as normal. She received hydrocortisone 100 mg IV at
induction as a surgical stress dose (Table 32.3) [17].
She did not require a muscle relaxant for intubation. If
rapid sequence induction was deemed necessary, a higher
dose of succinylcholine (1.5–2 mg/kg) would have been
required. This is possibly due to the reduced number of
ACh receptors at the neuromuscular junction. Onset of
succinylcholine is slower and the effect may be prolonged
due to concurrent therapy with cholinesterase inhibitors,
which hinders its clearance [34]. Non-depolarizing muscle
relaxants (NMDRs) should be avoided or titrated slowly
because of extreme sensitivity and unpredictable effects.
The response to NDMR can be variable even among
patients with only ocular symptoms or those in remission.
Monitoring with quantitative train-of-four testing is rec-
ommended when NMDRs are used. Reversal with neostig-
mine should be avoided, as this can precipitate a
cholinergic crisis, which can be difficult to distinguish
from myasthenic crisis. This is a manifestation of its mus-
carinic effects, including nausea, vomiting, abdominal
cramps, diarrhea, miosis, lacrimation, bronchospasm,
increased bronchial secretions, diaphoresis, and brady-
cardia [10]. Sugammadex has been suggested as the opti-
mal reversal agent when rocuronium or vecuronium is
used, as it does not have muscarinic effects. One case
series reports successful block reversal with 2–4 mg/kg,
depending on block intensity [35].
True/False Questions
1. (a) Myasthenia gravis is an autoimmune disorder affect-
ing the presynaptic membrane of the neuromuscular
junction
(b) Ten percent of MG patients are seronegative for
antibodies
(c) Early symptoms of MG include diplopia and ptosis
(d) The Tensilon test is routinely performed to confirm
diagnosis
(e) Symptoms of MG are usually worse in the morning
- (a) Anticholinesterase agents should be discontinued 1
week before surgery
(b) A myasthenic crisis is caused by ventilatory muscle
insufficiency or weakness of the upper airway
muscles
(c) Stage 1 of the Modified Osserman and Genkins clas-
sification signifies the most severe disease
(d) The Manual Muscle Testing score is best used for
assessing disease progression rather than severity
(e) Succinylcholine is contraindicated in MG patients
What Complications Is the Patient with Prior Ischemic Stroke Subject to in the Perioperative Period?
• Ischemic stroke
• Acute myocardial infarction
• Cardiovascular death
• Bleeding secondary to antithrombotic or antiplatelet agents when continued perioperatively
What Evidence Is There That the Patient with a History of Ischemic Stroke Is at Increased Perioperative Risk for a Repeat Ischemic Stroke?
• The largest study to date to evaluate the association between recent ischemic stroke and perioperative complications found a strong time-dependent relationship between prior ischemic stroke and adverse postoperative outcome [1].
- This was a retrospective cohort study of nearly half a million noncardiac procedures.
-Perioperative stroke occurred in 11.9% of patients with a history of
ischemic stroke if surgery was performed within the first 3 months of the cerebrovascular event compared to a 0.1% perioperative stroke rate in those without a history of stroke.
- This risk decreased as the interval from stroke to surgery increased, stabilizing at approximately 9 months, although still higher at this time point than in those patients with no history of stroke.
-The risk was the same regardless of whether the surgery was low, intermediate, or high risk. The authors of this large cohort study
suggested that patients with a history of recent ischemic stroke should be considered at increased perioperative risk until 9 months have elapsed since the event.
• In an analysis of 47,750 patients undergoing noncarotiid major vascular surgery, a history of cerebrovascular disease (history of stroke with or without residual deficit, TIA, or preoperative hemiplegia) was found to be the risk factor most strongly associated with postoperative stroke [2]
What Other Factors Are Known to Increase the Risk of Perioperative Stroke?
○ Analysis of 523,059 noncardiac, non-neurologic patients in the American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP®) database showed additional independent predictors for perioperative stroke: age ≥ 62 years, hypertension requiring therapy, myocardial infarction within 6 months of surgery, acute renal failure, pre-existing dialysis, COPD, and current tobacco use.
Does Beta-Blockade Increase the Risk of Perioperative Stroke?
○ According to the Perioperative Ischemic Evaluation (POISE) trial, introduction of metoprolol in the immediate preoperative period reduced cardiac death and nonfatal myocardial infarction/cardiac arrest [4]. However, the incidence of all-cause mortality and stroke increased.
○ Subsequent retrospective studies have looked at patients on
chronic beta-blocker therapy.
- In a large retrospective study, continued use of metoprolol preoperatively in noncardiac surgery was associated with a fourfold increase in periop-
erative stroke [5]. There was a significantly higher incidence of stroke in patients taking preoperative metoprolol compared with those taking atenolol [5].
- A single-center cohort study of 44,092 consecutive patients demonstrated
that perioperative metoprolol and atenolol were both associated with an increased risk of perioperative stroke when compared to the more β1-specific bisoprolol [6].
- A recent Cochrane review concluded that in noncardiac surgery, the
evidence shows an increase in death and a potential increase in stroke rate with the use of beta-blockers [7].
○ Overall, the evidence was deemed to be low to moderate in quality, not
allowing definitive conclusions to be established. Knowing the risks associated with acute beta-blocker withdrawal, current practice is to continue beta-blockade in the perioperative period in those patients on established therapy. De novo initiation of beta-blockade preoperatively is not recommended.
What Is the Precise Definition of Perioperative Stroke?
○ Perioperative stroke includes any stroke, whether embolic, thrombotic, or hemorrhagic, occurring intra-operatively or within 30 days of surgery, that results in motor, sensory, or cognitive dysfunction that persists for ≥24 hours.
○ The majority of perioperative strokes are ischemic in nature and associated with systemic atherosclerosis.
What Is the Risk of Perioperative Stroke in the General Population?
○ The overall risk of clinically apparent perioperative stroke for noncardiac, non-neurological surgery ranges from 0.1% to 0.8%.
○ The incidence varies for type of surgery and presence of associated risk factors.
○ Data from the ACS NSQIP database found that, when cardiac and neurological surgical procedures were excluded, the overall incidence of
perioperative stroke to be 0.1% [3].
○ Another investigation using ACS NSQIP data found that patients undergoing non-carotid major vascular surgery had a 0.6% incidence of peri-operative stroke
Is Perioperative Stroke Always Clinically Obvious?
○ Covert perioperative strokes have no clinical symptoms or signs but are evident on magnetic resonance imaging of the brain.
○ A prospective cohort study of patients undergoing elective noncardiac surgery found that 7% of patients had a perioperative covert stroke.
○ Given the lack of clinical signs, these may be erroneously mistaken for insignificant events. However, in this study, 42% of patients with a covert
stroke experienced cognitive decline at 1 year following surgery compared to 29% of those in the control group.
○ Increased postoperative delirium and overt stroke or transient ischemic attacks at 1 year were also associated with presence of perioperative covert stroke.
What Are the Consequences of a Perioperative Stroke?
○ The occurrence of a perioperative stroke has significant effects on morbidity and mortality.
○ The ACS NSQIP review of noncardiac non-neurological procedures demonstrated that perioperative stroke caused significant morbidity and mortality and was associated with an eightfold increase in mortality within 30 days.
○ Review of noncarotid major vascular surgeries from the ACS NSQIP database found that perioperative stroke was associated with a threefold increase in 30-day mortality as well as increased length of hospital
stay.
○ More recently in a retrospective analysis of 4,264,963 surgical procedures identified from the Nationwide Inpatient Sample (NIS) over an 11-year period, perioperative stroke was an independent predictor of 30-day in-hospital morbidity and mortality.
- It was also an independent predictor of length of hospital stay beyond 14 days, cardiovascular and pulmonary complications as well as in-
hospital mortality
What Is the Optimal Time Interval Between Ischemic Stroke and Surgery?
○ As highlighted in the large cohort study from Jørgensen et al. outlined above, the first 3 months following the cerebrovascular event pose the greatest risk for further stroke in the perioperative period.
○ At 9 months post event, the risk appears to have stabilized but is still higher than for those with no prior history of ischemic stroke. The recently published consensus statement from the Society for Neuroscience in Anesthesiology and Critical Care (SNACC) supports considering delaying elective surgery for 9 months after the stroke event.
How Should Patients with a History of Stroke or Transient Ischemic Attack Be Evaluated Preoperatively?
○ It is standard practice following a nondisabling stroke or transient ischemic attack for patients to be evaluated by a physician with stroke expertise.
○ Investigations undertaken as part of this assessment which should be reviewed preoperatively include brain imaging with noninvasive vascular imaging, laboratory tests including screening for diabetes and dyslipidemia, and a 12-lead ECG.
○ Holter ECG monitoring and an echocardiography may have been undertaken if a cardiac embolic mechanism was suspected.
○ Review of these findings, if available, is helpful in determining the mechanism and extent of injury.
○ For patients with a remote history of stroke and who have been stable for many years, a discussion of recurrent stroke risk is appropriate and should be documented.
○ Patients who have had a stroke within the previous 9 months should be fully informed of risk, with the timing and urgency of the elective procedure the subject of multidisciplinary consensus.
○ Thorough preoperative evaluation will enable risk factors for perioperative stroke to be identified and optimized within the given time frame, e.g., hypertension, hyperlipidemia, myocardial ischemia, renal impairment, diabetes, COPD, and smoking.
What Is the Optimal Blood Pressure Target in the Ischemic Stroke Patient?
○ Hypertension is the single most important modifiable risk factor for stroke. ○ The American Heart Association currently recommends a target blood pressure below 140/90 mmHg in previously untreated hypertensive patients who suffer a stroke/TIA, while a systolic blood pressure target of <130 mmHg may be reasonable in adults who have suffered a lacunar stroke.
Should Aspirin Be Held Perioperatively in the Patient with a History of Stroke or Transient Ischemic Attack?
○ The decision to stop or continue aspirin in the perioperative period depends on the indication for aspirin, the risk of thromboembolism, the proposed surgery, and its associated risk of postoperative bleeding.
○ Previous concerns regarding the preoperative cessation of aspirin were based on concerns about the prothrombotic effect of surgery and the rebound procoagulant response to abrupt termination of therapy.
○ The POISE-2 trial, however, found that perioperative aspirin administration did not affect the primary outcomes of death or myocardial infarction after noncardiac surgery.
○ There was no difference in the incidence of stroke: 0.3% in the aspirin treatment group versus 0.4% in the placebo group (p = 0.62). On the other hand, major bleeding occurred in 4.6% of the aspirin group versus 3.8% of the treatment group (p = 0.04).
○ Currently, there is no evidence to support the continuation of perioperative aspirin to reduce perioperative stroke in noncardiac surgery.
○ Present guidelines recommend discontinuing aspirin 7–10 days prior to elective or nonurgent noncardiac surgery, except in patients with recent coronary stenting or those undergoing carotid endarterectomy .
○ Perioperative guidelines for aspirin in patients undergoing carotid endarterectomy are outlined in Chap. 10.
How Is Perioperative Anticoagulation Managed in Patients with Atrial Fibrillation Being Treated with a Direct Oral Anticoagulant After Ischemic Stroke?
○ Direct (non-vitamin K) oral anticoagulants (DOACs) are preferred over warfarin for nonvalvular atrial fibrillation.
○ A pragmatic approach to perioperative DOAC interruption takes account of surgical bleeding risk (Table 33.1) [19–21], renal function, and DOAC type.
○ Patients with creatinine clearance greater than 50 ml/min should have DOACs held for 2 days before surgery with a high risk of bleeding and for 1 day before surgery with a low bleeding risk.
○ Patients with a creatinine clearance of 30–50 ml/min and having surgery with a high bleeding risk should have dabigatran held for 4 days before surgery and anti Xa inhibitors, e.g., rivaroxaban, apixaban, and edoxaban held for 2 days.
○ Patients with a creatinine clearance of 30–50 ml/min and having surgery with a low bleeding risk should have dabigatran held for 2 days before surgery and anti Xa inhibitors held for 1 day. The difference can be accounted for by the longer half-life of dabigatran, i.e., up to 18 hours with normal renal function and up to 23 hours with reduced creatinine clearance.
○ Timing of DOAC interruption corresponds to three to four half-lives for surgical procedures with low bleeding risk and four to five half-lives for high
bleeding risk procedures.
○ Bridging with low molecular weight heparin (LMWH) is not required in most cases due to the much more rapid offset and onset times for DOACs compared with warfarin.
- Furthermore, an observational study of patients with atrial fibrillation being treated with dabigatran showed significantly more major bleeding in the group who were bridged with LMWH perioperatively compared to those who did not receive bridging therapy, and there was not a significant difference in thromboembolic events.
How Is Anticoagulation with Warfarin
Managed Perioperatively?
Warfarin is the anticoagulant of choice in patients with a
mechanical heart valve and moderate to severe mitral steno-
sis [18]. The bleeding risk for the surgical procedure should
first be decided and the need for bridging therapy evaluated.
Patient stratification for thromboembolic risk adapted from
the American College of Chest Physicians Clinical Practice
Guidelines is shown in Table 33.2 [21, 24, 25]. If warfarin is
indicated for atrial fibrillation, the need for heparin bridging
therapy will be dependent on the CHADS2 score (see Chap.
6 on atrial fibrillation).
Where cessation of warfarin therapy is deemed appropri-
ate, it should be omitted for 5 days preoperatively. If bridg-
ing therapy with subcutaneous low molecular weight heparin
or intravenous unfractionated heparin is indicated, this
should be commenced on the third preoperative day. The last
dose of subcutaneous low molecular weight heparin should
be administered on the morning of the day before surgery.
Only half of the daily dose should be administered.
Should the Patient’s Ramipril Be Continued
Perioperatively?
Angiotensin-converting enzyme inhibitors and angiotensin
II receptor blockers should be held on the day of surgery due
to their well-documented association with perioperative
hypotension [
Should Statin Therapy Be Continued Perioperatively?
○ The use of statins in primary and secondary prevention of stroke is irrefutable.
○ Statin therapy is therefore started or recommenced following all ischemic strokes or TIAs.
○ Benefits of perioperative statin therapy in patients undergoing carotid endarterectomy include reduced in-hospital mortality, stroke, and long-term protection against MI .
○ The discontinuation of statin therapy has been shown to increase risk of myocardial infarction following major vascular surgery [29].
○ The VISION study, a large international, prospective, cohort study in patients undergoing noncardiac surgery, demonstrated that preoperative statin therapy was independently associated with a lower risk of cardiovascular outcomes at 30 days. The relative risk of stroke at 30 days was 0.83 in patients being treated with a statin.
○ Although there are no large randomized trials, it seems prudent, in light of what has been shown, to continue statin therapy through-out the perioperative period including on the day of surgery for those patients already established on therapy.
How Is MS Diagnosed?
• Clinical diagnosis is supported by MRI and CSF findings.
• Clinical features suggestive of MS are outlined in Table 35.1 [2, 4].
• The McDonald criteria are a set of clinical, radiological, and laboratory diagnostic guidelines for diagnosis of MS
○ These criteria can be used to diagnose both relapsing-remitting at the first clinical attack or primary progressive MS [5].
• Lesions separated in space (radiographically) and time are essential elements of the McDonald criteria.
• MRI features used to diagnose MS include one or more lesions, representing demyelinated plaques, disseminated in space in regions susceptible to demyelination, e.g., periventricular white matter, cerebral cortex, cerebellum, or spinal cord.
• CSF analysis for presence of oligoclonal bands can be used to confirm the diagnosis if there are doubts regarding dissemination in space and time
What Drugs Are Used for Management of MS?
Pharmacological therapy for MS is non-curative.
However, MS patients may be on a variety of agents for
(a) symptom control;
(b) treatment of acute exacerbations;
(c) reduction of relapse frequency, duration, and accumulation of brain lesions for patients with relapsing remitting disease; and d) treatment
of progressive MS. A general approach to these drug categories and specific agents is outlined in Table 35.2 [6, 7].
What Are the Perioperative Implications of Drugs Used for Treatment of MS?
Disease-modifying drugs have numerous associated side
effects that may have perioperative implications. These are
summarized in Table 35.3
