Additional Information
Book Details
Abstract
A guide to imaging for common neurological problems
Tourette's syndrome
Restless legs syndrome
Diagnosis and management of transient ischaemic attack and ischaemic stroke in the acute phase
The management of spasticity in adults
Post-acute care and secondary prevention after ischaemic stroke
Posterior circulation ischaemic stroke
First seizures in adults
Drug treatment of epilepsy in adults
Management of chronic epilepsy
Frontotemporal dementia
Chronic migraine
Pharmacological prevention of migraine
Cluster headache
Thunderclap headache
Trigeminal neuralgia
Polymyalgia rheumatica
Neuropathic pain: mechanisms and their clinical implications
Painful diabetic neuropathy
Fibromyalgia
Management of chronic pain in older adults
Cancer induced bone pain
Table of Contents
| Section Title | Page | Action | Price |
|---|---|---|---|
| Book Cover | C | ||
| Title | i | ||
| Copyright | ii | ||
| About the publisher | iii | ||
| About The BMJ | iii | ||
| Contents | iv | ||
| About the editors | vi | ||
| Introduction to Neurology and Pain | vii | ||
| Diagnosis and management of transient ischaemic attack and ischaemic stroke in the acute phase | 1 | ||
| What is an acute cerebrovascular event? | 1 | ||
| Is it an acute cerebrovascular event? | 2 | ||
| Clinical diagnosis | 2 | ||
| Imaging | 2 | ||
| Other investigations | 2 | ||
| How should I approach suspected TIA? | 2 | ||
| How will specialist services manage the patient with suspected stroke or TIA? | 3 | ||
| Patients with TIA | 3 | ||
| Patients with acute ischaemic stroke | 4 | ||
| Aspirin | 4 | ||
| Thrombolysis | 4 | ||
| Surgical intervention | 5 | ||
| Physiological monitoring and other treatments | 5 | ||
| Post-acute care and secondary prevention after ischaemic stroke | 7 | ||
| How should I assess a patient who has survived a stroke? | 7 | ||
| What kind of care should be delivered in hospital? | 8 | ||
| Evidence of benefit of stroke units | 8 | ||
| What makes a stroke unit? | 8 | ||
| Prevention of venous thrombosis | 8 | ||
| Feeding patients | 8 | ||
| Mobilisation: how soon? | 9 | ||
| Facilitating discharge | 9 | ||
| Antithrombotic following ischaemic stroke | 9 | ||
| How are common complications treated after stroke? | 10 | ||
| What measures help to prevent another stroke? | 11 | ||
| Management of carotid disease | 11 | ||
| How to manage hypertension | 11 | ||
| Treating high cholesterol, diabetes and lifestyle risks | 12 | ||
| Posterior circulation ischaemic stroke | 14 | ||
| What is posterior circulation ischaemic stroke? | 14 | ||
| What causes posterior circulation stroke? | 14 | ||
| What are the clinical symptoms and signs of posterior circulation ischaemia? | 15 | ||
| Which other disorders can mimic posterior circulation ischaemic stroke? | 16 | ||
| Stroke chameleons | 16 | ||
| Which clinical syndromes are caused by posterior circulation stroke? | 16 | ||
| How is posterior circulation ischaemic stroke diagnosed? | 17 | ||
| How is posterior circulation stroke managed? | 18 | ||
| Thrombolysis | 18 | ||
| Acute endovascular therapy | 18 | ||
| Neurosurgery | 19 | ||
| Which investigations are needed after treatment of posterior circulation stroke? | 19 | ||
| What treatment is recommended after posterior circulation stroke? | 19 | ||
| Which patients are at highest risk of deterioration or recurrence after posterior circulation minor stroke or TIA? | 20 | ||
| What is on the horizon for posterior circulation stroke? | 21 | ||
| The management of spasticity in adults | 23 | ||
| What is spasticity? | 23 | ||
| What are the clinical features of spasticity? | 23 | ||
| What is the differential diagnosis of spasticity? | 23 | ||
| How is spasticity assessed? | 23 | ||
| Approach to adults presenting with new onset spasticity | 24 | ||
| Approach to adults presenting with worsening of spasticity | 24 | ||
| When should a patient with spasticity be referred? | 24 | ||
| What is the impact of spasticity? | 25 | ||
| What is the aim of the management of spasticity? | 25 | ||
| What are the non-drug interventions for spasticity? | 25 | ||
| Stretching and splinting | 25 | ||
| Postural management and standing | 26 | ||
| Exercises | 26 | ||
| Other physical modalities | 26 | ||
| What are the drug interventions for spasticity? | 26 | ||
| Oral antispasticity drugs | 26 | ||
| Cannabinoids | 27 | ||
| Botulinum toxin | 27 | ||
| Intrathecal baclofen | 28 | ||
| Chemical neurolysis | 28 | ||
| First seizures in adults | 30 | ||
| How common are first seizures? | 30 | ||
| Diagnosing a first seizure: how do people present? | 30 | ||
| Seizures without loss of consciousness | 30 | ||
| Myoclonus | 30 | ||
| Aura (simple partial subjective seizure) | 31 | ||
| Simple partial motor seizure | 31 | ||
| Seizures with loss of consciousness | 31 | ||
| Absences | 31 | ||
| Complex partial seizure | 31 | ||
| Tonic-clonic seizure (convulsion) | 31 | ||
| Differential diagnosis of transient loss of consciousness | 31 | ||
| Syncope | 31 | ||
| Non-epileptic attack disorder | 32 | ||
| Should first status epilepticus and seizure clusters be considered first seizure or epilepsy? | 32 | ||
| Who is most at risk? | 32 | ||
| How should first seizure be managed? | 32 | ||
| Why is investigation after first seizure important? | 32 | ||
| What investigations are needed after first seizure in acute setting? | 33 | ||
| What investigations will be done at early specialist follow-up? | 33 | ||
| Is brain imaging needed in all first seizure patients? | 33 | ||
| Is this a first seizure and will it recur? | 33 | ||
| To treat or not to treat? | 34 | ||
| Does early treatment improve long term prognosis and prevent death? | 34 | ||
| Should we treat if provocation is ongoing? | 34 | ||
| What follow-up is recommended after first seizure? | 34 | ||
| What should we advise with regards to driving? | 34 | ||
| What advice should be given about safety at home and at leisure? | 35 | ||
| What advice should be given regarding sex following first seizure? | 35 | ||
| Should we warn all patients about sudden unexpected death in epilepsy? | 35 | ||
| Drug treatment of epilepsy in adults | 37 | ||
| Introduction | 37 | ||
| Epidemiology | 37 | ||
| When to start treatment | 37 | ||
| Selecting the first antiepileptic drug | 38 | ||
| Effectiveness in new onset epilepsy | 38 | ||
| Tolerability and safety of drugs in new onset epilepsy | 41 | ||
| Optimizing drug regimens | 44 | ||
| Drug resistant epilepsy | 44 | ||
| Failure of the first drug to induce sustained seizure remission and drug resistant epilepsy | 45 | ||
| Treatment of special patient groups | 46 | ||
| Women | 46 | ||
| Pregnant women and neonates | 46 | ||
| Older people | 46 | ||
| Patients with comorbidities | 47 | ||
| Patients with status epilepticus and prolonged acute convulsive seizures | 48 | ||
| Stopping antiepileptic drugs | 48 | ||
| Emerging treatments | 49 | ||
| Barriers to the development of new drugs for drug resistant epilepsy | 49 | ||
| Conclusions | 49 | ||
| Management of chronic epilepsy | 53 | ||
| Who gets epilepsy? | 53 | ||
| What is the goal of epilepsy treatment? | 53 | ||
| How is epilepsy managed? | 53 | ||
| What affects seizure control and prognosis in chronic epilepsy? | 54 | ||
| What are the factors to consider if seizure control is suboptimal? | 55 | ||
| Is the diagnosis correct? | 55 | ||
| Is the drug treatment appropriate? | 55 | ||
| What other medications and illnesses need to be considered? | 55 | ||
| Is adherence to treatment adequate? | 55 | ||
| Has the patient had a good trial with a maximally tolerated dose of all major antiepileptic drugs? | 55 | ||
| Which drug should the patient try next? | 56 | ||
| How can the total drug load be minimised? | 56 | ||
| What about epilepsy surgery? | 56 | ||
| How often should people with epilepsy be reviewed? | 56 | ||
| What should an epilepsy review include? | 56 | ||
| Pharmacological aspects | 56 | ||
| Non-pharmacological aspects | 56 | ||
| Chronic migraine | 58 | ||
| Introduction | 58 | ||
| Epidemiology | 58 | ||
| Transformation and reversion factors | 59 | ||
| Individual and societal effects | 59 | ||
| Pathophysiology | 60 | ||
| Diagnosis | 60 | ||
| History and examination | 60 | ||
| Differentiating chronic migraine from other primary headaches | 61 | ||
| Comorbid conditions | 61 | ||
| Treatment | 61 | ||
| Risk factor modification and trigger avoidance | 62 | ||
| Prophylaxis | 62 | ||
| Drug with high quality evidence (>2 randomized placebo controlled trials) | 62 | ||
| Drugs with lower quality evidence (1 randomized trial) | 62 | ||
| Drugs used for both episodic migraine and chronic migraine | 63 | ||
| Non-drug treatments | 63 | ||
| Refractory chronic migraine | 63 | ||
| Topics to discuss with patients | 63 | ||
| Active participation in treatment | 63 | ||
| Avoid drug overuse | 63 | ||
| Be patient with prophylactic treatments | 63 | ||
| The goal is control | 63 | ||
| Looking ahead | 64 | ||
| Research | 64 | ||
| Future drug treatments | 64 | ||
| Future non-drug treatments | 64 | ||
| Chronic migraine guidelines | 64 | ||
| Chronic migraine diagnostic criteria | 64 | ||
| Defining refractory chronic migraine | 65 | ||
| Management | 65 | ||
| Clinical trial design for studies of chronic migraine | 65 | ||
| Conclusions | 65 | ||
| Pharmacological prevention of migraine | 68 | ||
| When to consider prevention for migraine | 68 | ||
| What are the goals of preventive treatment? | 68 | ||
| What do the treatments prevent? | 68 | ||
| What drugs are available for the prevention of migraine? | 68 | ||
| β blockers | 68 | ||
| Calcium channel blockers | 69 | ||
| Other antihypertensive drugs | 69 | ||
| Antidepressants | 69 | ||
| Antiepileptic drugs | 69 | ||
| Supplements and herbs | 70 | ||
| Other drugs | 70 | ||
| Botulinum toxin A | 70 | ||
| Combination treatment | 70 | ||
| When should preventive treatment be discontinued? | 70 | ||
| Cluster headache | 72 | ||
| What is cluster headache? | 72 | ||
| Who gets it? | 72 | ||
| How is cluster headache diagnosed? | 72 | ||
| Where is the pain and what is it like? | 73 | ||
| How long does an attack last? | 73 | ||
| How often do individual attacks occur? | 74 | ||
| Which other symptoms occur with the attack? | 74 | ||
| Does anything trigger the attacks? | 74 | ||
| How often do bouts of attacks occur? | 74 | ||
| Which conditions resemble cluster headache? | 75 | ||
| How should patients with cluster headache be managed? | 75 | ||
| Treatment of individual attacks | 75 | ||
| Oxygen | 75 | ||
| Triptans | 75 | ||
| Preventive treatment | 75 | ||
| Nerve blocks and infusions | 76 | ||
| Neuromodulation | 76 | ||
| Thunderclap headache | 78 | ||
| What is a thunderclap headache? | 78 | ||
| How should a patient with thunderclap headache be assessed? | 78 | ||
| What are the most common causes? | 78 | ||
| Subarachnoid haemorrhage | 78 | ||
| Reversible cerebral vasoconstriction syndrome | 79 | ||
| What are the less common causes of thunderclap headache? | 80 | ||
| Causes detected by plain CT or lumbar puncture | 80 | ||
| Causes that can be missed by plain CT and lumbar puncture | 81 | ||
| Which investigations are needed? | 81 | ||
| When is four vessel cerebral angiography still necessary? | 82 | ||
| What about primary headache disorders as a cause of thunderclap headache? | 82 | ||
| Restless legs syndrome | 83 | ||
| What is it? | 83 | ||
| Who gets it? | 83 | ||
| What causes restless legs syndrome? | 84 | ||
| What else could it be? | 84 | ||
| What impact does restless legs syndrome have on health? | 84 | ||
| How is restless legs syndrome managed? | 85 | ||
| What problems are associated with dopamine agonists? | 85 | ||
| How do I choose between different dopamine agonists? | 85 | ||
| What other drugs are available? | 86 | ||
| Whom should I refer to a specialist? | 86 | ||
| Neuropathic pain: mechanisms and their clinical implications | 88 | ||
| Introduction | 88 | ||
| Rationale for mechanism based treatment | 88 | ||
| Search methods | 88 | ||
| Physiology and classification | 89 | ||
| Emotional versus physiological aspects | 90 | ||
| Peripheral mechanisms | 92 | ||
| Peripheral sensitization | 92 | ||
| Expression of ion channels | 92 | ||
| Phenotypic switch | 92 | ||
| Sensory denervation and sprouting of collateral nerve fibers | 92 | ||
| Sympathetically maintained pain | 93 | ||
| Spinal mechanisms | 94 | ||
| Spinal glutamatergic regulation | 94 | ||
| Glial activation and proinflammatory cytokines | 94 | ||
| Supraspinal mechanisms | 95 | ||
| Disinhibition | 96 | ||
| Spinal cord level | 96 | ||
| Supraspinal level | 96 | ||
| Neuropathic versus nociceptive pain: different entities or part of the same continuum? | 96 | ||
| Emerging treatments | 97 | ||
| Conclusions | 97 | ||
| Management of lumbar spinal stenosis | 100 | ||
| Introduction | 100 | ||
| Incidence and prevalence | 100 | ||
| Sources and selection criteria | 100 | ||
| Definition | 100 | ||
| Causes | 101 | ||
| Symptoms and signs | 101 | ||
| Natural course of LSS | 102 | ||
| Pathophysiology | 102 | ||
| Diagnosis | 102 | ||
| Electrodiagnostics | 103 | ||
| Imaging | 103 | ||
| Clinical prediction rules | 103 | ||
| Management | 104 | ||
| Non-surgical options | 104 | ||
| Drugs | 104 | ||
| Physiotherapy | 104 | ||
| Injections | 105 | ||
| Other non-surgical options | 105 | ||
| Surgical options | 105 | ||
| Decompression | 105 | ||
| Role of postoperative rehabilitation | 106 | ||
| Role of fusion | 106 | ||
| Interspinous spacers | 107 | ||
| The MILD procedure | 107 | ||
| Associated conditions affecting treatment | 107 | ||
| Degenerative spondylolisthesis | 107 | ||
| Degenerative scoliosis | 108 | ||
| Conclusion | 108 | ||
| Opioids for low back pain | 112 | ||
| Introduction | 112 | ||
| Sources and selection criteria | 112 | ||
| Incidence and prevalence of low back pain | 112 | ||
| Prevalence of symptoms | 112 | ||
| Prevalence of pathophysiologic changes | 113 | ||
| Trends in opioid prescribing | 113 | ||
| Efficacy and effectiveness of opioids for low back pain | 113 | ||
| Acute low back pain | 113 | ||
| Chronic low back pain | 114 | ||
| Opioids versus placebo | 114 | ||
| Opioids versus other drugs | 114 | ||
| Observational studies for chronic back pain | 115 | ||
| Reasons for potential loss of efficacy | 115 | ||
| Responses to opioid tapering | 115 | ||
| Adverse effects of opioid treatment for low back pain | 116 | ||
| Opioid dependency, misuse, and addiction | 116 | ||
| Dependency | 116 | ||
| Problem use of prescription opioids | 116 | ||
| Prevalence of problem use | 117 | ||
| Overdose and mortality risks | 117 | ||
| Other adverse effects | 118 | ||
| Sedation and dizziness | 118 | ||
| Depression | 118 | ||
| Endocrine effects | 118 | ||
| Interference with other treatments | 118 | ||
| Reducing risks of opioid therapy | 118 | ||
| Screening | 118 | ||
| Newer safety strategies | 119 | ||
| Prescription drug monitoring programs | 119 | ||
| Reformulation | 120 | ||
| Emerging treatments | 120 | ||
| Guidelines | 120 | ||
| Conclusion | 120 | ||
| Trigeminal neuralgia | 124 | ||
| How common is trigeminal neuralgia? | 124 | ||
| Who are most at risk of having trigeminal neuralgia? | 124 | ||
| What is the underlying pathophysiology of trigeminal neuralgia? | 124 | ||
| How is trigeminal neuralgia diagnosed? | 124 | ||
| What investigations should be done? | 125 | ||
| Imaging | 125 | ||
| Biochemical investigations | 126 | ||
| What are the medical options for treatment? | 126 | ||
| What are the surgical options? | 127 | ||
| What to do in a crisis? | 128 | ||
| What other support is available for patients with trigeminal neuralgia? | 129 | ||
| Painful diabetic neuropathy | 131 | ||
| Introduction | 131 | ||
| Epidemiology | 131 | ||
| Classification | 131 | ||
| Diagnostic studies | 132 | ||
| Important patient outcomes | 133 | ||
| Treatment | 134 | ||
| Prevention | 134 | ||
| Symptoms | 134 | ||
| Antiepileptic drugs | 134 | ||
| Antidepressants with effects on norepinephrine reuptake | 134 | ||
| Opioid based drugs | 134 | ||
| α lipoic acid | 135 | ||
| Topical treatments | 135 | ||
| Non-pharmacologic treatments | 135 | ||
| Summary of evidence on treatment | 135 | ||
| Guidelines and recommendations | 135 | ||
| What to discuss with patients | 136 | ||
| Challenging assumptions in diabetic neuropathy | 136 | ||
| Unresolved questions and emerging treatments | 136 | ||
| Conclusions | 137 | ||
| Fibromyalgia | 140 | ||
| What is fibromyalgia and how common is it? | 140 | ||
| Who gets fibromyalgia? | 140 | ||
| What causes fibromyalgia? | 141 | ||
| Why and how should fibromyalgia be diagnosed? | 141 | ||
| Treatment of fibromyalgia | 142 | ||
| What is the role of non-drug treatments? | 142 | ||
| Physical therapies (active) | 143 | ||
| Physical therapies (passive) | 143 | ||
| Acupuncture | 143 | ||
| Psychological therapies | 143 | ||
| How effective are drugs in the treatment of fibromyalgia? | 144 | ||
| Analgesics | 144 | ||
| Opioids | 144 | ||
| Antidepressant drugs | 144 | ||
| Anticonvulsant drugs | 145 | ||
| Other drugs | 146 | ||
| How strong is the evidence from clinical trials in fibromyalgia? | 146 | ||
| Complex regional pain syndrome | 148 | ||
| Introduction | 148 | ||
| Incidence | 148 | ||
| Incidence in the general population | 148 | ||
| Incidence after injury | 149 | ||
| Sources and selection criteria | 149 | ||
| Pathophysiology | 149 | ||
| Factors related to the initiating injury | 149 | ||
| Central and peripheral nociceptive sensitization | 150 | ||
| Altered sympathetic nervous system function and sympatho-afferent coupling | 151 | ||
| Inflammatory and immune related factors | 151 | ||
| Brain changes | 151 | ||
| Genetic factors | 152 | ||
| Psychological factors | 152 | ||
| Natural course of CRPS | 152 | ||
| Acute CRPS | 152 | ||
| Chronic CRPS | 153 | ||
| Delayed healing versus emerging CRPS | 153 | ||
| Warm and cold CRPS | 153 | ||
| Traditional CPRS stages | 153 | ||
| CPRS spread | 153 | ||
| Diagnosis | 154 | ||
| Treatment | 154 | ||
| Drug treatment | 155 | ||
| Ganglion blocks | 155 | ||
| Spinal cord stimulation | 156 | ||
| Psychological interventions | 156 | ||
| Can CRPS be prevented? | 156 | ||
| Vitamin C | 156 | ||
| Ischemic reperfusion injury | 156 | ||
| CRPS in children | 156 | ||
| Emerging treatments | 156 | ||
| Guidelines | 156 | ||
| Conclusion | 157 | ||
| Polymyalgia rheumatica | 161 | ||
| What is polymyalgia rheumatica? | 161 | ||
| What are the objective abnormalities in polymyalgia rheumatica? | 161 | ||
| Can polymyalgia rheumatica “overlap” with other rheumatological disorders? | 161 | ||
| Association with giant cell arteritis | 161 | ||
| Overlap with rheumatoid arthritis | 162 | ||
| Genetic heterogeneity | 162 | ||
| How is polymyalgia rheumatica diagnosed? | 162 | ||
| How can the classic clinical features of polymyalgia rheumatica be identified? | 162 | ||
| What further investigations are recommended before starting glucocorticoids? | 163 | ||
| When should glucocorticoids be started? | 163 | ||
| When and how should the glucocorticoid dose be tapered? | 164 | ||
| What if patients cannot tolerate glucocorticoid withdrawal even years later? | 164 | ||
| What are the risks of long term glucocorticoids and how can they be reduced? | 165 | ||
| What is the prognosis in polymyalgia rheumatica? | 165 | ||
| Temporomandibular disorders | 168 | ||
| What are TMDs? | 168 | ||
| How common are TMDs and who gets them? | 168 | ||
| What causes TMDs? | 168 | ||
| What are the clinical features? | 169 | ||
| How are TMDs diagnosed? | 169 | ||
| Axis 1 | 169 | ||
| Axis 2 | 170 | ||
| What are the red flags? | 170 | ||
| What makes TMDs more likely to become a chronic musculoskeletal pain? | 170 | ||
| What is the management? | 170 | ||
| Reversible and conservative treatments | 170 | ||
| Irreversible approaches | 172 | ||
| Why is psychological management of TMDs important? | 172 | ||
| Management of chronic pain in older adults | 176 | ||
| What is chronic pain and how is it caused? | 176 | ||
| Who gets it? | 176 | ||
| How are older patients with chronic pain assessed? | 176 | ||
| History | 177 | ||
| Examination | 177 | ||
| Imaging | 177 | ||
| Assessing pain in older patients with major cognitive impairment | 177 | ||
| What is the approach to management? | 178 | ||
| Social aspects of management | 179 | ||
| Home visits | 179 | ||
| What drug interventions are available? | 180 | ||
| Paracetamol | 180 | ||
| Non-steroidal anti-inflammatory drugs | 180 | ||
| Opioids | 180 | ||
| What psychological interventions are available? | 181 | ||
| Cognitive behavioral therapy | 181 | ||
| Self management programs | 181 | ||
| What rehabilitative and exercise approaches are available? | 181 | ||
| When should patients be referred to a pain specialist? | 182 | ||
| What is the role of mobile health technology? | 182 | ||
| What limitations exist in the evidence base about treatment? | 182 | ||
| Cancer induced bone pain | 184 | ||
| What is cancer induced bone pain? | 184 | ||
| Who gets cancer induced bone pain? | 184 | ||
| What are the clinical features of cancer induced bone pain? | 184 | ||
| How is cancer induced bone pain initially managed? | 185 | ||
| Non-drug interventions | 185 | ||
| World Health Organization pain ladder | 185 | ||
| Strong opioids | 186 | ||
| Other drug interventions | 186 | ||
| What further treatment options are available? | 187 | ||
| Radiotherapy | 187 | ||
| Radioisotopes | 187 | ||
| Bisphosphonates | 187 | ||
| Denosumab | 187 | ||
| Interventional procedures | 187 | ||
| Surgery | 187 | ||
| Complementary therapies | 188 | ||
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