Neurology

Chapter 3 Neurology



Neurology and neuromuscular disorders




Epilepsy


Affects 1/200 of the general population. Continue anticonvulsants perioperatively.



Anaesthetic problems



• Enzyme induction. Chronic medication induces hepatic enzymes with resistance to i.v. induction agents and volatiles.

• Risk of seizures. Particularly with enflurane in a hypocapnic patient, methohexitone, ketamine and etomidate. Although propofol has not been demonstrated to cause significant EEG changes, excitatory phenomena are more common. Because patients risk losing their driving licence after an epileptiform event, it is recommended to avoid propofol in patients who are driving. Several case reports document successful use of propofol for the treatment of status epilepticus.

• Underlying pathology causing epilepsy.


Cerebrovascular disease


A cerebrovascular accident (CVA) is defined as a rapidly evolving episode of loss of cerebral function with symptoms lasting more than 24 h (<24 h = transient ischaemic attack) or leading to death. Annual incidence is 1–2/1000 in the UK, with a mortality of 15–30%.


Risk of perioperative stroke following general surgery is 0.2–0.7% in patients without a history of cerebrovascular disease. Most CVAs occur 2–10 days postoperatively, with an average of 7 days, and have an associated mortality of 26%. In those with a history of cerebrovascular disease, the risk is 2.9% with a mortality of 60%.


Risk factors include age, systolic hypertension, atrial fibrillation (AF), peripheral vascular disease and diabetes. Hyperextension or rotation of the patients neck during head surgery may reduce flow in vertebral and internal carotid arteries.



Preventative measures


Preoperative measures include treating risk factors and anticoagulation for patients in AF. The European Carotid Surgery Trial (ECST) and the North American Symptomatic Carotid Endarterectomy Trial (NACEST) suggest that carotid endarterectomy would benefit symptomatic patients with >70% carotid stenosis. Surgery should be deferred for 4–6 weeks after an acute event.


Intraoperative measures. Avoid hypocapnia (steal syndrome) or hypercapnia (inverse steal syndrome), avoid hypo- or hyperglycaemia, and avoid extreme cervical spine rotation or extension. Maintain BP within normal range.


Postoperative measures. Avoid hypotension, dehydration and hypoxia.



Parkinsons disease


Disorder of the extrapyramidal system with degeneration of dopaminergic neurones in the substantia nigra of the basal ganglia, giving rise to intention tremor, ‘cogwheel’ rigidity, akinesia and postural changes. Dysautonomia also common (orthostatic hypotension, urinary dysfunction, sleep disorders). Prevalence 1% in those >65 years age. First described as ‘the shaking palsy’ by James Parkinson in 1817.


Patients are already confused in a strange environment, which is worsened by GA. Patients are often difficult to assess preoperatively, with reduced pulmonary function, upper airway obstruction, weakness and incoordination of inspiratory and expiratory muscles. The usual drug regimen should be continued preoperatively. If patient is well controlled on l-DOPA, both general and regional anaesthesia is usually well tolerated. Avoid drugs that exacerbate Parkinson’s (phenothiazines, droperidol, metoclopramide).


Continue anti-Parkinsonian medication immediately postoperatively, via nasogastric (NG) tube if necessary. Delayed mobilization postoperatively increases risk of respiratory complications and deep vein thrombosis (DVT). Avoid antiemetics that are dopamine antagonists (e.g. prochlorperazine), although all may cause extrapyramidal and movement disorders.



Multiple sclerosis (MS)


Chronic progressive demyelinating disease characterized by repeated exacerbations and partial remissions. Affects 1:2000; equal incidence in both sexes. Upper motor neurone lesions, cerebellar lesions and sensory deficits are common.


General anaesthesia does not exacerbate MS. Use normal doses of muscle relaxants.


Regional blockade. New lesions may develop coincidentally at the time of regional blockade and subsequent symptoms may be difficult to differentiate from nerve injury or may be blamed on the block. Therefore regional blockade is relatively contraindicated.



Motor neurone disease


Progressive degeneration of motor function with sparing of higher mental function and sensory function. Involves both upper and lower motor neurones. Progressive muscle atrophy, spasticity, pseudobulbar palsy. Affects smooth, striated and cardiac muscle.


General anaesthesia. Risk of aspiration from delayed gastric emptying and bulbar weakness. Weak respiratory muscles. Suxamethonium may cause hyperkalaemia. Increased sensitivity to non-depolarizing relaxants and induction agents.


Regional anaesthesia. Avoid impairment of respiratory muscles but otherwise safe.



Autoimmune disease



Myasthenia gravis


Affects 1:20 000. A result of autoantibodies directed against the neuromuscular junction. Ocular, facial, bulbar and limb weakness in 85% of patients.


Preoperative. Continue anticholinesterases and steroids. Intubate if vital capacity falls below 1000 mL. Consider β-blockers and atropine to stabilize the autonomic nervous system.


GA. Greatly increased sensitivity to non-depolarizers; decreased sensitivity to depolarizing blockers. Give conventional anticholinesterase dose at end of surgery and then restart anticholinesterases at a decreased dose. Extubate when inspiratory pressure >−30 cmH2O or FVC >15 mL.kg−1.


Postoperative. Risk factors for postoperative ventilation are:


• disease for >6 years

• chronic respiratory disease

• pyridostigmine >750 mg.day−1

• FVC <2.9 L.


Eaton–Lambert syndrome


Severe muscle weakness found in association with 1% of patients with bronchial carcinoma, thyroid disease and connective tissue disorders (systemic lupus erythematosus, polyarteritis nodosa). Unlike myasthenia gravis, causes proximal rather than bulbar weakness, muscle power increases with exercise and no fade occurs on tetanic stimulation.


Increased sensitivity to both non-depolarizing and depolarizing blockers.


Associated with ↑ ACTH (hypertension, diabetes) and ↑ PTH (↑ Ca2+, dehydration).



Myotonia



Myotonic dystrophy


Affects 1:25 000. Autosomal dominant. Myotonia with difficulty releasing hand grip, muscle weakness, cataracts, ‘inverted smile’, bilateral ptosis, frontal balding, masseter and sternomastoid wasting, and bulbar weakness (aspiration and chest infections); also cardiac conduction defects, cardiomyopathy, valve defects, obstructive sleep apnoea, dysphagia and reduced gastric emptying.


Sensitivity to sedatives, induction agents (barbiturates, propofol), opioids and non-depolarizing neuromuscular blockers. Anticholinesterases, cold and shivering may worsen myotonia. Suxamethonium may produce a generalized myotonic response. Non-depolarizing relaxants are safe. Myotonic contraction with surgical diathermy may be a major problem. Postoperative complications are usually related to cardiac pathology or muscle weakness leading to aspiration. Postoperative shivering may induce a myotonic crisis.


Pregnancy may exacerbate myotonia and muscle weakness.



Myotonia congenita (Thomsen’s disease)


Affects 1:25 000. Autosomal dominant. Generalized muscular hypertrophy, stiffness on initiating movement, relieved by exercise. Myotonia may be severe but no muscle weakness. Anaesthetic problems are as for myotonic dystrophy. Association with malignant hyperthermia.



Familial periodic paralysis



Hyperkalaemic periodic paralysis


Episodes of flaccid paralysis associated with hyperkalaemia. Paralysis may occur with potassium levels no greater than 4.0 mmol, possibly due to a defect in the sarcolemma causing spontaneous depolarization. Triggered by stress, cold, hunger and exercise. Vital to avoid hyperkalaemia perioperatively, using insulin/dextrose and loop diuretics. Suxamethonium may cause sufficient hyperkalaemia to precipitate an attack.



Hypokalaemic periodic paralysis


Unrelated to hyperkalaemic periodic paralysis. Asymmetric paralysis involving arms, legs, trunk and neck. Usually spares diaphragm and facial muscles. Associated with reduced cell membrane potential, making muscle more excitable. Precipitated by heavy carbohydrate meals, diuretics, alkalosis and hypothermia. The effect of muscle relaxants may be clinically similar to the paralysis itself.



Bibliography



Berrouschot J., Baumann I., Kalischewski P., et al. Therapy of myasthenic crisis. Crit Care Med. 1997;25:1228-1235.


Eriksson L.I. Neuromuscular disorders and anaesthesia. Curr Opin Anaesth. 1995;8:275-281.


Errington D.R., Severn A.M., Meara J. Parkinson’s disease. BJA CEPD Rev. 2002;2:69-73.


Kam P.C.A., Calcroft R.M. Perioperative stroke in general surgical patients. Anaesthesia. 1997;52:879-883.


Le Corre F., Plaud B. Neuromuscular disorders. Curr Opin Anaesth. 1998;11:333-337.


Nicholson G., Pereira A.C., Hall G.M. Parkinson’s disease and anaesthesia. Br J Anaesth. 2002;89:904-916.


Sneyd J.R. Propofol and epilepsy. Br J Anaesth. 1999;82:168-169.


Thavasothy M., Hirsch N. Myasthenia gravis. BJA CEPD Rev. 2002;2:88-90.



Neuroanaesthesia




Physiology



Cerebrospinal fluid (CSF)


Secreted by the choroid plexus in the lateral, III and IV ventricles. Flows through foramen of Magendie and Lushka and is absorbed by arachnoid villi: 720 mL.day−1. Contents are:


• pH 7.3

• CSF >plasma: Na+, Cl−, Mg2+

• CSF <plasma: K+, HCO3−, glucose, protein.


Intracranial pressure (ICP)


Munro–Kelly hypothesis (1852) stated that the contents of cranium are not compressible (60% water, 40% solid). Therefore, increasing the volume within the cranium causes a rapid increase in pressure (Fig. 3.1).


image

Figure 3.1 Theoretical intracranial pressure–volume relationship.


However, compression of veins and communication of CSF with spinal column result in a small range of compensation before pressure increases (Fig. 3.2).


image

Figure 3.2 Actual intracranial pressure–volume relationship.


Normal CSF pressure = 0–10 mmHg. Neurosurgical patients often have raised ICP and so are already on the steep part of curve. Active treatment is needed if ICP >25–30 mmHg. CSF pressure oscillates with arterial pulse and swings with respiration.


Cushing reflex. Increased ICP causes hypertension and bradycardia.



Coning


All coning causes an autonomic storm. High pulmonary artery pressures may then result in neurogenic pulmonary oedema. ECG changes are now thought to be indicative of myocardial ischaemia. Reduced ADH secretion causes diabetes insipidus. Metabolic response is similar to that of the stress response following surgery.


• Temporal (tentorial) coning. Ipsilateral III nerve palsy, ↓ consciousness, Cushing reflex, decerebrate rigidity

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Aug 28, 2016 | Posted by in ANESTHESIA | Comments Off on Neurology

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