Tremor, bradykinesia, rigidity and postural instability
Due to reduced dopaminergic activity in substantia nigra in basal ganglia while cholinergic activity remains unchanged
Drug therapy is aimed at increasing dopamine activity or decreasing acetylcholine activity in the brain
L-dopa is converted to dopamine within the brain
MAOIs reduce central breakdown of dopamine
Ergot derivatives (bromocriptine) stimulate dopamine receptors
Antimuscarinics (procyclidine) are used to treat tremor

Anaesthetic implications
Excessive salivation
aspiration risk (reflux)
Labile BP (drugs and dysautonomia)
Reparatory function may be compromised by rigidity
Urinary retention will cause confusion
No IV dopaminergic drugs are available so maintain GI function

Drugs to avoid
Antiemetics that produce extrapyramidal SEs - phenothiazines, dopamine antagonists, droperidol. Cyclizine, ondansetron and dexamethasone OK
Antipsychotics and antidepressants
Antihypertensives have exaggerated effects

Multiple sclerosis

Demyelinated plaques in brain and spinal cord
Onset begins in early adulthood
5% rapidly decline
Relapsing and remitting disease
Steroids and interferon lengthen remissions
Symptoms range from isolated visual disturbance to paralysis
Respiratory failure is end-stage
Demyelinated fibres are sensitive to heat (a 0.5
temp can worsening of symptoms)

Document pre-existing neurology

GA does not effect disease
Neuraxial block has been associated with symptom recurrence but is a relative rather than absolute CI
Peripheral regional OK
Avoid sux as
NDMRs as normal
Autonomic instability


Chaotic brain dysfunction

History (seizure control, drivers licence)
U&E, glucose
Avoid prolonged fasting
Maintain anti-epileptic therapy
Can use benzodiazepine pre-med

Propofol and thiopentone both anti-epileptic. Propofol is associated with abnormal movements but not seizure activity on EEG
Use a non steroidal NMB. Anti-epileptic drugs are enzyme inducers so will metabolise steroidal drugs quickly
Avoid hypocarbia as this lowers seizure threshold
Use antiemetics unlikely to cause dystonias as this can be confused with seizures. Don’t use prochlorperazine, metoclopramide or droperidol.

Day case anaesthesia is suitable
Aim is for normal GI function and usual medications ASAP
Phenytoin and valproate available IV; carbemazapine PR

Cerebrovascular disease

Associated with hypertension, diabetes, smoking, obesity. These are of course causes of IHD and RF
Operation within 6/52 of an event is associated with x20 risk of perioperative stroke – delay for 3/12 if possible
Hemiplegia of <6/12 assoc with exaggerated hyperkalaemic response to sux

Measure BP both arms
Continue antihypertensives
Replace warfarin with heparin
Document any pre-existing neurological deficit
Ask about postural and neck movement symptoms (vertebrobasilar insufficiency)

BP likely to be labile due to stiff vasculature – induce carefully and avoid pressor response with alfentanil
Maintain BP at normal levels
Maintain neutral neck position
Avoid hypocapnia (

Myasthenia Gravis

Autoimmune destruction of post synaptic nicotinic receptors at NMJ
Causes weakness and fatigability
Any age but most common in young adult women
Associated with thymomas – thymectomy leads to improvement in symptoms even if normal thymus
Symptoms range from mild ptosis to bulbar palsy and respiratory failure
Treatment is oral anticholinesterase
Severe disease requires immunosuppression, plasmapheresis or IG infusion

Assess degree of weakness, duration of symptoms and effect of missing a dose anticholinesterase
Bulbar symptoms are predictive of post-op support
Maintain normal medication right up till surgery

Avoid NMBs if possible
If must use:
Sux 1.5mg/kg – bigger dose needed as less receptors. Reduced levels of plasma esterase (anticholinesterases and plasma pheresis) prolong its action so don’t give NDMR until muscle function returned
10% dose NDMR
Nerve stimulator
Should be reversible with normal doses neostigmine if pre-op control good
Avoidance of reversal is preferred to avoid overdose with further doses and cholinergic crisis (salivation, diarrhoea, bronchorroea)
NGT if bulbar palsy
Regional anaesthesia to reduce need for morphine

Normal oral meds (NGT may be needed) or IV neostigmine

Drugs dependent on esterases for elimination
Sux, remi, esmolol, mivacurium, ester LAs

Myaesthenic syndrome assoc with cancer (often lung)
Proximal weakness

Motor neuron disease

Degenerative disorder of upper and lower motor neurons in spinal cord
Weakness, atrophy and fasciculations progressing to bulbar palsy
Relentless course with death from respiratory failure in 3 years
Mental competency remains

Anaesthetic considerations
Autonomic dysfunction
Aspiration risk
Respiratory failure post-op
Avoid sux
Monitor NDMRs with nerve stimulator

Dystropohia myotonica

Autosomal dominant
Pre-frontal balding and cataracts
Presents in 2
nd or 3rd decade
Atrophy of skeletal, cardiac and smooth muscle
Skeletal muscle
Persistent contraction after voluntary use or stimulation
Weakness and loss of central drive
Cardiomyopathy, arrhythmias, block
Bulbar palsy
Mental retardation
DM, hypothyroid, hypoadrenal

Cardiorespiratory status

Sux CI
Avoid NMB if poss
Neostigmine and nerve stimulator can
muscle contraction
Regional anaesthesia does not prevent muscle contraction
Keep warm (shivering
Induction agents and opiates can have exaggerated effects


Other Muscular dystrophies

Range of congenital muscular disorders characterised by progressive weakness of various muscle groups
Most severe is Duchenne’s which causes cardiorespiratory failure and death by 25yrs
Assoc with MH

Autonomic Neuropathy

Nutritional deficiencies

Signs and symptoms
Postural hypotension
Abnormal valsalva
Loss of sinus arrhythmia
Labile BP
Silent ischaemia
Loss of response to hypoglycaemia
Erratic temperature control
Gastric stasis

Anaesthetic considerations
Exaggerated hypotension on induction
aspiration risk
Tolerate changes in positioning poorly
Temperature control
Tolerate hypovolaemia poorly