Perioperative Stroke and Cognitive Decline in Non-Cardiovascular (General) Surgery –A Review

  1. William E. Wallis M.D.,F.R.A.C.P.

Perioperative Stroke and Cognitive Decline in Non-Cardiovascular (General) Surgery –A Review


1. In contrast to cardiovascular surgery, the literature on perioperative stroke in general surgery is sparse

2. The risk of stroke for most general surgery varies from 0.08 to 0.7%, but higher with pulmonary, head/ neck, and peripheral vascular surgery; as well as with patient’s vascular risk factors (1-6).

3. Risk factors are multiple and the expected. For example, the incidence increases with age: 0.1–0.2% for age 65 years, 0.5% for age 65–74 years and 1.0% for age > 75 years.

4. Not all strokes occur during surgery. Around 45% of perioperative strokes are recognised in first 24 hrs post of and remaining 55% later (2). In one report (3) the median postop time of stroke was 2 days. In another series (4), 53% occurred within 24 hours, 31% within one to seven days, and 16% within seven to thirty-six days.

5. Despite widely-held view to the contrary, surgical hypotension and cerebral hypoperfusion are not the most common causes of perioperative stroke (1-6). In the absence of the obvious, such as AF, it is likely that a hypercoagulable state, akin to that related to postop pulmonary emboli, is the culprit. This may explain delay in many cases, as abnormal clotting can persist for 14 to 21 days postop (2). Imaging usually suggests an embolic cause (2), which may be in turn related to a hypercoagulable state (2).

6. Risk-benefit balance of withdrawing antiplatelet agents and anticoagulants before surgery is as yet uncertain but guidelines exist (1,10,11)

7. Perioperative stroke mortality rate is high 18-26% (1, 2).

8. Transient postoperative cognitive decline is common and age-related (7-9), but long-term dementia probably does not occur (9)

9. Prevention of perioperative stroke in general surgery is not as yet evidence-based.


References 

1. Macellari F et al.. Perioperative Stroke Risk in Nonvascular Surgery. Cerebrovasc Dis. 2012;34:175–181

2. Selim,M. Perioperative stroke. N Engl J Med. 2007;356:706-13

3. Limburg, M et al. Ischemic stroke after surgical procedures: clinical features, neuroimaging, and

risk factors. Neurology. 1998;50:895-901.

4. Wong,D. Perioperative stroke. Part 1: general surgery, carotid disease, and carotid

endarterectomy. Can J Anaesth. 1991;38:347-73.

5. Ng,J et al. Perioperative stroke in noncardiac, nonneurosurgical surgery. Anesthesiology.

2011;115:879-90.

6. Bateman,B et al. Perioperative acute ischemic stroke in noncardiac and nonvascular surgery:

incidences, risk factors, and outcomes. Anesthesiology. 2009;110:231-8.

7. Monk,T et al. Predictors of cognitive dysfunction after major noncardiac surgery. Anesthesiology.

2008;108:18-30.

8. Newman,S et al. Postoperative cognitive dysfunction after noncardiac surgery: a systematic

review. Anesthesiology. 2007;106:572-90.

9. Steinmetz,J et al. Is postoperative cognitive dysfunction a risk factor for dementia? A cohort

follow-up study. Br J Anaesth. 2013 Jun;110 Suppl 1:i92-7

10. Armstrong M et al., Summary of evidence-based guideline: Periprocedural management of

antithrombotic medications in patients with ischemic cerebrovascular disease: Report of the

Guideline Development Subcommittee of the American Academy of Neurology. 2013 80:2065-2069

11. P.J. Devereaux et al. Aspirin in Patients Undergoing Noncardiac Surgery N Engl J Med, March 31,

2014



Placebos from St Jerome to functional MRI

Literature Review of Neuralgic Amytrophy (NA) (Brachial neuritis)


Neurology Journal Club
9.9.10
W Wallis

Literature Review of Neuralgic Amytrophy (NA)
(Brachial neuritis)

2 cases G Knight and TI case

General
Brachial neuritis is a relatively uncommon neuromuscular disorder. Known by 20 terms, but NA or Parsonage-Turner Syndrome are than brachial neuritis.  The annual incidence is estimated to be 1.64 cases per 100,000 population (Beghi et al 1985). The male-to-female ratio was approximately 2:1 in this study, but it has varied from 1.6:1 to 10.5:1 in different hospital-based series (Magee and Dejong 1960; Tsairis et al 1972; Devathasan and Tong 1980). Although cases have been reported at all ages (3 months to 71 years), the disease seems to be most prevalent in the 20- to 50-year-old age group (Parsonage and Turner 1948; Gathier and Bruyn 1970; Beghi et al 1985). INA is rare in children. Van Alfen and colleagues described 2 patients (aged 5 months and 4 years and 8 months, respectively) and reviewed literature on neuralgic amyotrophy in childhood (younger than 16 years of age). There appears to be higher incidence of painless brachial neuritis and poorer prognosis as compared to the adult forms. The childhood variety should be distinguished from hereditary neuralgic amyotrophy and acute poliomyelitis (van Alfen et al 2000).

Epidemiology
Brachial neuritis is a sporadic disorder, but occasional epidemic clusters have been reported (Bardos and Somodska 1961). In a retrospective study of nontraumatic brachial plexopathies, neuralgic amyotrophy constituted 48% of the cases (Mullins et al 2007).

Phenotype
In its initial stages, brachial neuritis may be misdiagnosed as a painful musculoskeletal disorder..Brachial neuritis, characterized by acute pain and weakness with variable atrophy and sensory loss around the shoulder girdle, is a fairly well-defined clinical entity.   The onset of illness is heralded by acute pain across the shoulder, often awakening the patient at night. The pain is severe and constant, described as sharp, aching, boring, or throbbing, and radiates to the outer aspect of the arm, neck, axilla, or forearm. It is aggravated by movement of the arm but not by coughing or sneezing. Consequently, the arm is held in a position of adduction and internal rotation at the shoulder and flexion at the elbow (the flexion-adduction sign) (Aymond et al 1989). The pain is usually localized above the elbow; when prominent below the elbow, it is likely to be associated with involvement of the lower brachial plexus or its component nerves (England and Sumner 1987). Infrequently, the pain occurs bilaterally and rarely may be absent in an otherwise typical case of brachial neuritis. The duration of pain varies from a few days to several months.

Muscle weakness appears within a few days to weeks. The exact onset may be difficult to determine because of restricted mobility of the limb due to pain. The upper brachial plexus is commonly affected, and the deficit may correspond to 1 or more nerve roots, trunks, cords, or peripheral nerves. The severity of muscle weakness is variable. Muscle stretch reflexes are impaired or absent in weakened muscles, and prominent muscle atrophy ensues. The deltoid, serratus anterior, spinati, biceps, triceps, and wrist and finger extensor muscles can be affected in that order, and in various combinations, although a recent study of 246 cases noted that spinati were the most frequently involved muscles (van Alfen and van Engelen 2006). Weakness may be confined to the muscles innervated by individual nerves (eg, suprascapular, long thoracic, or axillary) or 1 branch of the nerve (eg, isolated involvement of supraspinatus, infraspinatus, brachialis, or flexor pollicis longus muscle) (Magee and Dejong 1960; Tsairis et al 1972; England and Sumner 1987; Cruz-Martinez et al 2002).

Sensory loss is usually inconspicuous, partly because the upper brachial plexus gives rise mostly to motor nerves. Hypesthesia is often confined to a small area on the outer aspect of the upper arm in the distribution of the axillary nerve or along the radial surface of the forearm and base of the thumb

Although the clinical picture of brachial neuritis is characteristic, the localization of the lesion is puzzling, and the pathogenesis of the disorder is unknown. Localization to the region of brachial plexus does not explain several clinical and electrodiagnostic observations, eg, (1) isolated involvement of nerves such as long thoracic, spinal accessory, or phrenic, which exit from the nerve roots proximal to the plexus; (2) severe denervation in the distribution of nerves arising from 1 part of the plexus with sparing of other nerves from the same trunk or cord; and (3) dissociated involvement of muscles supplied by the same nerve. Overall, 4 patterns of involvement can be identified: (1) mononeuropathy, (2) mononeuropathy multiplex, (3) plexus with mononeuropathy, or (4) multiple combinations (Cwik et al 1990). Such findings can be attributed to a lesion distally in the peripheral nerves or a discrete proximal lesion of the fascicular fibers destined to constitute those nerves (Spillane 1943; Wilbourn 1985; England and Sumner 1987). The essential underlying process seems to be multifocal; it may remain localized to 1 part of the brachial plexus or its component nerves, or it may become widespread.

Variations of Phenotype:
The phenotype of both idiopathic (INA) and hereditary (HNA) neuralgic amytrophy is more varied than previously recognised.  Usual phenotypes are as above. Others:

Under-appreciated variations of the syndrome include:
Cranial Nerve involvement
Bilateral brachial involvement (28%)
Lumbosacral
Phrenic nerve 7% 17/33 cases idiopathic P nerve palsy assoc with NA
Cranial nerves 9,10,11,12. Particularly CN 9.
Sensory usually lateral antebrachial cutaneous or median nerves
.  
Antecedent or Precipitating Events:
A variety of antecedent and precipitating factors have been recognized in all large series and case reports, but their role in the causation of the disease has not been elucidated, and the aetiology of sporadic brachial neuritis remains unknown. The antecedent factors can be classified into (1) infections: nonspecific viral illnesses, influenza, Coxsackie virus, Epstein-Barr virus, Q fever, Mycoplasma pneumoniae, bacterial pneumoniae, typhoid, syphilis, HIV disease, and Lyme borreliosis (Parsonage and Turner 1948; Tsairis et al 1972; Botella et al 1997; Post et al 2002; Tsao et al 2004; Wendling et al 2009); (2) immunizations: tetanus toxoid, diphtheria, swine flu, immune sera, and recombinant DNA hepatitis B vaccination (Reutens et al 1990; Stratton et al 1994); (3) surgery and child birth (Dumitru and Liles 1989; Malamut et al 1994; Lederman and Wilbourn 1996); and (4) miscellaneous: strenuous exercise, lumbar puncture, radiologic contrast administration, allergy desensitization, intravenous cytarabine, heroin addiction, severe asthma, interferon therapy, botulinum toxin injection for writer's cramp, and thrombolytic therapy with streptokinase (Subramony 1988; Mulvey et al 1993; Wilbourn 1993; Sheean et al 1995). Brachial neuritis may rarely be associated with Hodgkin disease or develop following chemotherapy (Symonds et al 1994). A single case due to a hypersensitivity reaction to lamotrigine has been noted (Hennessy et al 1998)
Surgery:
Common precipitating factor for NA.  Recognised by Parsonage and Turner 1948. 14% of cases in largest series of 246 cases   
Other less appreciated phenomena:
  1. Less satisfactory recovery than expected. Almost a third of patients suffer from chronic pain, and the majority of both INA and HNA patients exhibit persisting functional deficits after an average follow-up of >6 years. The recovery rate was slow in most patients
  2. A high recurrence rate even in the non-hereditary or idiopathic form of NA (INA).
  3. Persistent and disabling pain. 3 phases. The ini only tial phase of continuous severe pain lasting 3 to 4 weeks is followed by stabbing sharp pain and is then replaced by a musculoskeletal type of pain that may persist for several months or years

Idiopathic (INA) vs hereditary (HNA) NA
There are similarities and differences between INA and the hereditary form of neuralgic amytrophy (HNA).   A familial form of brachial neuritis is inherited as a dominant trait. Recurrent attacks. In the familial form of disease the male-to-female ratio is 1:1, cases occur at a younger age than in the sporadic form of the disease, and bilateral involvement is more common. Atypical features such as cranial nerve involvement, lumbosacral plexopathy, and mononeuropathies occur more frequently in the familial form of illness. A large clinical study of 199 patients with idiopathic neuralgic amyotrophy and 46 patients with hereditary neuralgic amyotrophy confirmed the above features and also noted a more severe paresis and poorer functional outcome in familial variety (van Alfen and van Engelen 2006). Hereditary neuralgic amyotrophy has been linked to chromosome 17q25, and further studies have shown mutations in the septin (SEPT9) gene (Kuhlenbaumer et al 2005).
Aetiology
Although the aetiology is repeatedly considered to be “autoimmune” the evidence for this is indirect and unsatisfactory.  If it is autoimmune, it is odd that the majority of the patients with the condition are men rather than women, although there are some examples of “autoimmune” disorders where men outnumber women (Goodpasture syndrome). A variety of antecedent and precipitating factors have been recognized in all large series and case reports, but their role in the causation of the disease has not been elucidated, and the etiology of sporadic brachial neuritis remains unknown. The antecedent factors can be classified into (1) infections: nonspecific viral illnesses, influenza, Coxsackie virus, Epstein-Barr virus, Q fever, Mycoplasma pneumoniae, bacterial pneumoniae, typhoid, syphilis, HIV disease, and Lyme borreliosis (Parsonage and Turner 1948; Tsairis et al 1972; Botella et al 1997; Post et al 2002; Tsao et al 2004; Wendling et al 2009); (2) immunizations: tetanus toxoid, diphtheria, swine flu, immune sera, and recombinant DNA hepatitis B vaccination (Reutens et al 1990; Stratton et al 1994); (3) surgery and child birth (Dumitru and Liles 1989; Malamut et al 1994; Lederman and Wilbourn 1996); and (4) miscellaneous: strenuous exercise, lumbar puncture, radiologic contrast administration, allergy desensitization, intravenous cytarabine, heroin addiction, severe asthma, interferon therapy, botulinum toxin injection for writer's cramp, and thrombolytic therapy with streptokinase (Subramony 1988; Mulvey et al 1993; Wilbourn 1993; Sheean et al 1995). Brachial neuritis may rarely be associated with Hodgkin disease or develop following chemotherapy (Symonds et al 1994). A single case due to a hypersensitivity reaction to lamotrigine has been noted (Hennessy et al 1998).
Pathology
The pathology of this disorder is variable, but it is likely a mononeuritis multiplex with predilection for brachial and lumbosacral plexuses. Based on the temporal relationship of these events to the onset of disease, autoimmune mechanisms have been postulated; however, evidence to support this hypothesis is scanty. Oligoclonal bands in the CSF and lymphocyte sensitization to brachial plexus nerves have been demonstrated, suggesting an immune-mediated process (Pierre et al 1990; Sierra et al 1991). A report of multifocal mononuclear infiltrates in brachial plexus biopsies from 4 patients with brachial neuritis further supports an immune basis (Suarez et al 1996). Based on the evidence of a variety of antecedent factors, autoimmune or infectious mechanisms have been considered; however, no definite laboratory evidence supports these etiologies. Pierre and colleagues found oligoclonal bands in the CSF and raised serum IgG titers against Herpes simplex and varicella-zoster virus; these findings suggested that reactivation of virus was involved in the pathogenesis of the disease (Pierre et al 1990). Some evidence of immune-mediated process has been observed in the form of altered lymphocyte subsets, with a decrease in CD3 values and an increase in the CD4:CD8 ratio. Increased blastogenic activity of lymphocytes was observed in cultures containing extracts from brachial plexus nerves but not from the sacral plexus; serratus anterior paralysis was correlated with the blastogenic response to an extract from the long thoracic nerve (Sierra et al 1991).

Pathologic studies are limited to occasional radial cutaneous nerve biopsies, which reveal axonal degeneration. Cusimano and colleagues reported 2 patients with recurrent brachial plexus neuropathy who developed palpable, painful supraclavicular masses (Cusimano et al 1988). There was fusiform swelling of the nerves on surgical exploration, and excisional biopsy revealed focal chronic inflammation, extensive onion bulb formation, endoneurial edema, and tubuloreticular endothelial inclusions. Sierra et al 1991). A report of multifocal mononuclear infiltrates in brachial plexus biopsies from 4 patients with brachial neuritis further supports an immune basis (Suarez et al 1996).

Investigations:
The electrophysiology is variable. Abnormal findings include decreased amplitude of sensory nerve action potential and compound muscle action potential, denervation in appropriate muscles, and sometimes prolonged distal latency (Flaggman and Kelly 1980; England and Sumner 1987). Abnormal sensory potentials and a normal paraspinal muscle EMG help distinguish a brachial plexus lesion from spinal nerve root involvement. EMG findings are, thus, consistent with a predominant axonal involvement in brachial neuritis. However, demyelinative changes, eg, motor conduction block in proximal segments, have been reported. These may resolve completely, but persistent conduction deficits can occur (Lo and Mills 1999; Watson et al 2001).
Many patients have non-specific blood test and spinal fluid abnormalities.  Some also have enhancement of the brachial plexus visible on MR imaging.
Treatment
The treatment of the condition remains uncertain, but there is some evidence that early treatment with steroids may have at least a short-term beneficial effect.  It is not known, however, where it has long-term effect in terms of disability.



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References

Reference 1:  Dhand,UR.  Brachial neuritis.  MedLink Neurology (11August 2009 ).
Reference 2:  van Alfen,N and van Englen,G.  The clinical spectrum of neuralgic amytrophy in 246 cases.  Brain 2006;129:438-450.
Parsonage MJ, Turner JW. Neuralgic amyotrophy, the shoulder girdle syndrome. Lancet 1948;1:973-8.
Reference 3:  Park,P et al.  Brachial neuritis: an under-recognised loss of upper extremity paresis after cervical decompression surgery.  Spine.  2007;32:640-644.
Reference 4:  Szwejbka,P et al.  Bilateral anterior interosseous neuropathy following surgery: a case report.  Electromyogr Clin Neurophysiol.  2004;44:183-6.
Reference 5:  Simon,J and Fabry,G.  Parsonage-Turner syndrome after total hip arthroplasty.  J Arthroplasty.  2001;16:518-20.
Reference 6:  Squintani,G et al.  Unusual Parsonage-Turner syndrome with relapses in bilateral simultaneous anterior interosseous neuropathy.  Neurol Sci 2009;30:513-6.
Reference 7:  Malamut,R et al.  Postsurgical idiopathic brachial neuritis.  Muscle Nerve. 1994;17:320-4.
Reference 8:  Ueda,M et al.  Phenotypic spectrum of hereditary neuralgic amytrophy caused by the SEPT9 R88W mutation.  JNNP. 2010;81:94-6.
Tsao BE, Ostrovskiy DA, Wilbourn AJ, Shields RW Jr. Phrenic neuropathy due to neuralgic amyotrophy. Neurology 2006;66:1582-4.
Reference 9:  Ikegami,G et al.  Bilateral phrenic nerve paralysis manifested by orthopnea for six months in a patient with neuralgic amytrophy.  Inter Med.  2009;148:2123-7.
Pierre PA, Laterre CE, Van den Bergh PY. Neuralgic amyotrophy with involvement of cranial nerves IX, X, XI, and XII. Muscle Nerve 1990;13:704-7.
Reference 10:  Sanders,E et al.  Brachial plexus neuritis and recurrent laryngeal nerve palsy.  J Neurol. 1988;235:323
Seror P. Isolated sensory manifestations in neuralgic amyotrophy: report of eight cases. Muscle nerve 2004;29(1):134-8..
Reference 11:  van Alfen,N et al.  Treatment of idiopathic and hereditary neuralgic amytrophy (brachial neuritis).  Cochrane Database Syst Rev. 2009;3:CD006976.

Dr. Wallis publications in Neurology Journal

Dr Wallis's original medical publication on the Treatment of Epilepsy was cited by the prestigious medical journal Neurology as one of the Landmark Articles in the journal's 50 year history. It was also chosen as one of the 9 important articles on Epilepsy in the journal's 50 year history.





 




For more about Dr Wallis go to his Website