Amiodarone can also cause a destructive thyroiditis, releasing thyroid hormone into the circulation and causing hyperthyroidism. Treatment is with high-do se steroids Hypothyroidism \200 More common in areas with low iodine intake (up to 13 % incidence) \200 Diagnose with decreased free T3 and free T4 concentrations with elevated TSH concentrations An elevated TSH alone is not diagnostic \200\224 may be transient, especially in the \201 rst three months of treatment. If the patient is well, recheck in 3 months Amiodarone withdrawal is rarely necessary. Adding levothyroxine sodium will correct the problem 140 CHAPTER 6 Drugs Analgesia Older patients are more likely to suffer chronic pain than younger ones, owing to the increased frequency of conditions such as osteoarthritis, osteoporosis, etc. Pain management is more challenging and a standard \200\230pain ladder \200\231 approach n ot always useful because of the altered sensitivity of the older patient to certain classes of analgesic medication. Non-steroidal anti-in \202 ammatory drugs Includes aspirin (especially at analgesic doses) . Potential problems \200 Fluid retention causing worsening hypertension, cardiac failure, and ankle swelling Renal toxicity \200\224 risk of acute tubular necrosis, exacerbated by intercurrent infection, or dehydration Peptic ulceration and gastrointestinal bleeding \200\224 there is an increased risk with i ncreased age, and the bleeds tend to be more signi \201 cant 2The number of older patients requiring hospitalization because of NSAID-induced deteriorat ion in renal or cardiac function actually exceeds the number with gastrointestinal bleeds. \200 Age itself is probably not an independent risk factor for most complications of NSAID treatment, but factors such as comorbidities, co-medications, hydrat ion, nutritional status and frailty are linked to an increased risk, all of which are more common with advancing age Guidance for use in older patients \200 NSAIDs should be used with extreme caution in old er patients, and avoided altogether in the very frail \200 Should be given for a short period only \200 Use low-dose moderate potency NSAIDs (eg ibuprofen 0.6g/day) \200 Avoid using two NSAIDs together (this includes low-dose aspirin) \200 Consider co-prescription of a gastric-prot ective agent (eg omeprazole) for the duration of the therapy Avoid using ACE inhibitors and NSAIDs together \200\224 they have opposing effects on \202 uid handling, and are likely to cause renal toxicity in combination Opioid analgesia Wide range of drugs sharing many common features, but with qualitative and quantitative differences. Potential problems include constipation, nausea and vomiting, anorexia, confusion, drowsiness, and respiratory depression. Guidance for use in older patients \200 Most of these are dose dependant, and careful up- titration will obtain the right balance of analgesic effect and adverse effects Constipation is common (worse in older people) but can be managed with good bowel care Most adverse effects are reversible once the medication is reduced or discontinued ANALGESIA 141 HOW TO Manage pain in older patients Diagnose the cause Chronic abdominal pain may be due to constipation that will respond to bowel care rather than analgesia. Consider non-drug measures \200 Weight loss and physical activity helps with many pains ( eg arthritis) \200 Temperature treatments (eg hot/cold packs applied to painful joint) \200 TENS machines \200 Alternative therapies (eg acupuncture, aromatherapy) can help \200 Avoidance of (non-essential) activity that provokes pain if possible Consider targete d therapy For example: topical capsaicin for post-herpetic neuralgia, local nerve blocks fo r regional pain, massage for musculoskeletal pain, joint replace- ment for arthritic pain, or radiotherapy for pain from bony metastases Regular paracetamol \200 Well-tolerated and with few side effects \200 Before moving fr om this, ensure that the maximum dose is being taken regularly (ie 1g taken four times a da y) for optimal analgesic effect. Many patients will \201 nd taking an occasional paraceta mol ineffective \200\224 explain that regular dosing increases analgesic effect Opioid analgesia \200 Second line therapy in most older patients \200 Options to deal w ith mild (eg codeine, dihydrocodeine), moderate (eg tramadol) and severe pain (eg morphine, diamorphine, fentanyl) \200 Compound preparations are useful when adding an opioid to re gular paracetamol, as it limits the number of tablets taken. Co-codamol (codeine and parace tamol) has variable doses of codeine (8mg, 15mg, or 30mg per tablet) allowing up titration of the opioid component \200 All affect same receptors, so use as a continuum \200\224 i f regular maximum dose codeine is not working, then step up to the next level of opioid str ength (eg if 60mg codeine four times daily (qds) is not suf \201 cient then change to tram adol 50mg qds or morphine sulfate M/R 5mg bd) Various formulations for the delivery of strong opiates. Liquids are useful if there are swallowing problems (eg morphine sulfate solution). Slow-release ta blets (eg morphine sulfate M/R) and transdermal patches (eg fentanyl) provide constant anal gesic effect for continuous pain. Parenteral opiates are used in terminal care (subcutaneou s injections of morphine and diamorphine for intermittent pain; 24hr infusion pumps for con stant pain) \200 Monitor for side effects \200\224 active bowel care with initiation Oth er drug options \200 Very \201 t older patients can be given short courses of NSAIDs \200 Cyclo-oxygenase-2 (COX-2) inhibitors have a limited role Psychological factors \200 Depression is often coexistent (consequent or causal). Treatment can help with overall pain management Informal ( \200\230positive mental attitude \200\231) and formal psychotherapeutic approaches may be preferable to side effects of analgesic medication 142 CHAPTER 6 Drugs Steroids Oral steroids (usually prednisolone) are given for many conditions in older patien ts, commonly COPD exacerbation, polymyalgia rheumatica, rheumatoid arthritis, and colitis. Treatment may be long term. Although the bene \201 ts of treatment usually outweigh the ri sks, awareness of these can minimize harm. Discuss likely side effects with patients and ca rers. Cautions \200 Osteoporosis \200\224 this is most marked in the early stages of treatment . Older people will have diminishing bone reserves anyhow, and there is a strong argument for putting all steroid-treated older patients on bone protection at outset, unless the course is certain to be very short (eg less than 2 weeks). This should consist of daily calcium a nd vitamin D, along with a bisphosphonate (weekly preparations eg alendronate 70mg, improve concordance) Steroids can precipitate impaired glucose tolerance or frank diabetes . Monitor sugar level s periodically (eg weekly capillary blood sugar, or urinalysis) in all steroid users. Stero ids worsen control in known diabetics, necessitating more frequent monitoring Hypertension may develop because of the mineralocorticoid effect of prednisolone, and this should be checked for regularly Skin changes occur, and are particularly noticeable in older patients with less resilient skin. Purpura, bruising, thinning, and increased fragility are common Muscle weakness occurs with prolonged use, dominantly proximal in distribution. This leads to problems rising from chairs, climbing stairs etc. and may be the \201 nal straw for a frail older person with limited physical reserve. (See b \200\230Muscle symptoms \200\231, p.478) There is an increased susceptibility to infections on steroids, and the presentation may be less acute, making diagnosis more dif \201 cult. Candidiasis (oral and genital) is partic ularly common and should be treated promptly High doses (as used in treatment of giant cell arteritis) can cause acute confusion and sle ep disturbance , and older people are particularly prone. Give steroids in the morning if p ossible Cataracts may develop with long-term steroid use. If vision declines, look for cataracts wi th an ophthalmoscope and consider specialist referral Peritonitis may be masked by steroid use \200\224 the signs being less evident clinically. Have a higher index of suspicion of occult perforation in a steroid-treated older patient with abdominal pain. There is also a weak association between steroid use and peptic ulcera tion Adrenocortical suppression means that the stress response will be diminished in chronic steroid users. If such a patient becomes acutely unwell (eg septic), the exogenous steroid dose will need to be temporarily increased (eg double the usual oral dose, replace with intramuscular hydrocortisone if unable to take by mouth). Suppression ca n continue for months after stopping chronic steroids; have a low threshold for \200\230co vering \200\231 acute illness STEROIDS 143 Stopping treatment Many patients are on fairly low doses of steroids for a long period. It can be dif \201 cult to completely tail the dose, as steroid withdrawal effects (fevers, m yalgia, etc.) can often be mistaken for disease recurrence, and this often needs to be done very slowly (perhaps reducing by as little as 1mg a month). There is no such thing as a \200\230safe \200\231 dose of steroid so, for every patient you see on steroids, ask the fo llowing: \200 Can the dose be reduced? \200 Could a steroid sparing agent (eg azathiopr ine) be used instead? \200 Is the patient taking adequate bone protection? \200 What is the blood pressure and blood glucose? 144 CHAPTER 6 Drugs Warfarin Common indications range from absolute (PE, DVT, arti \201 cial heart valve repla cement) to relative (stroke prophylaxis in AF). Cautions \200 Risk is increased if the patient is unable to take medication reliably, so is not suitable without supervision for cognitively impaired patients, or those who self-ne glect. If there is an absolute indication, then consider supervised therapy (by spouse, fam ily, or carers via a dispensing system) or (rarely) a course of low molecular weight hepari n instead \200 Risk is higher if there is a high probability of trauma, eg recurrent fall s \200 Excess alcohol consumption is associated with poor concordance and falls. Liver en zymes are induced, making control of anticoagulation more dif \201 cult. Highly variable i ntake is especially problematic Comorbidity may increase sensitivity to warfarin (eg abnormal liver function, congestive ca rdiac failure) and should be screened for GPs will often be good judges of risk \200\224 consider discussing borderline cases Side effects \200 Bleeding is the major adverse event, ranging from an increased tendency to bruise to major life-threatening bleeds. The most signi \201 cant include intracerebra l hemorrhage and gastrointestinal blood loss. \200 Warfarin does not cause gastric irrita tion, but may accelerate blood loss from pre-existing bleeding sources. Ask carefully about history of non-steroidal use (including aspirin) and gastrointestinal symptoms (upper and lower). If any are presen t then quantify risk with further testing \200\224 full blood count and iron studies might indicate occult blood loss. If the warfarin is not essential, then a full gastrointestinal work-up may be appropriate before starting in the \201 tter patients. In frailer patient s, consider warfarin with empirical PPI Nosebleeds are common in older patients, and may become more signi \201 cant on warfarin. Often due to friable nasal vessels that are amenable to treatment by ENT surgeons, so reduc ing the risk of epistaxis on warfarin Reassessment of risk/bene \201 t balance \200 Patients often take warfarin for many year s \200 During that time, there is usually change in both the risk (serious bleeding) and the bene \201 t (reduced thromboembolism) of anticoagulation. The most commo n scenario is that the antithrombotic bene \201 t of anticoagulation remains, but that the bleeding risk increases and cannot be reduced \200\224 eg a patient falls frequently desp ite intervention, or has a major bleed that could recur (eg diverticular) Any drug must be stopped unless there is a net bene \201 t to the individual patient. In conjunction with patient (and carer), the indication for warfarin sh ould be reviewed periodically; perhaps annually in frail older people, and after any signi \201 cant event, eg hip fracture WARFARIN 145 Usual target international normalized ratio (INR) (See Table 6.2 .) Table 6.2 Target INRs Indication Target INR Duration Atrial \201 brillation 2.5 Lifelong Venous thromboembolism 2.5 Varies. Usually 6 months. Lifelong if recurrent or with ongoing precipitant (eg malignancy) . Shorter duration if identi \201 able precipitant and high bleeding risk 3.5 Lifelong Recurrent venous thrombo-embolism while on warfarin 3.5 Lifelong Mechanical prosthetic heart valves What to do when the INR is too high \200 Always look for the reason why the INR became el evated and correct this factor If there is no sign of bleeding, then stop warfarin and monitor the INR as it falls If the INR > 8 but there is no bleeding, a small dose of vitamin K (0.5 \200\2232.5mg) can be given to partially reverse the INR Do not give vitamin K routinely as control of anticoagulation will be made more dif \201 cult for weeks afterwards If there is bleeding, then the warfarin needs reversing with vitamin K and fresh frozen plasma For life-threatening bleeds (eg intracerebral hemorrhage) prothrombin complex concentrate can be used for rapid reversal 2If a patient bleeds at target INR, always consider the possibility of underlying serious d isease, eg bladder or gastrointestinal malignancy. Further reading British National Formulary . Oral anticoagulants section . Online: M www.bn f.org . 146 CHAPTER 6 Drugs HOW TO Initiate warfarin Discuss risks and bene \201 ts of treatment with the patien t \200\224 the indication is rarely absolute. Ensure the patient is told \200 There will be frequent blood tests and monitoring \200 Many medications interact with warfarin, so before taking any new medication (including ove r the counter), always check compatibility with the doctor, dentist, or pharmacist Use paracetamol or codeine-based analgesia (never NSAIDs) \200 Alcohol interacts with war farin metabolism, and should be taken in moderation and on a regular basis (avoid binge drinking) Vitamin K-containing foods (eg spinach) should not have variable intake If trauma occurs, bleeding may last longer. Apply pressure to wounds and seek medical help if it does not stop Give the patient an anticoagulant treatment book that will hold details of their treatment schedule and reinforce the information that you give them Induction \200 Check baseline clotting \200 Prescribe warfarin to be taken at 6pm \200 Medical notes should state indication, target INR, and duration of therapy The normal adult induction dose (10mg day 1, 10mg day 2, then an INR) is rarely appropriate in older patients who are more sensitive to its effects Reduce the dose if the patient is frail, has a low body weight, has multiple comorbidities, or a deranged baseline clotting \200 For most older patients 5mg /5mg /INR is a safer approach \200 If there are multiple factors causing concern, then 5m g /INR is better 2There is no rush. If the indication is absolute, then the patient should also be on therapeutic heparin until the INR is in range. It is much easier to increase the dose of warfarin, than to deal with bleeding from an overdose. \200 The INR will then ne ed checking daily, then alternate days until a pattern becomes clear Many hematology departments will offer automatic dosing with a schedule for retesting The INR testing can gradually be done less frequently, stretching to 12-weekly in long-term users Induction in hospital is now often done by anticoagulation teams WARFARIN 147 HOW TO Manage drug-induced skin rashes Common side effect in older patients \200\224 thought to be due to altered immune function. Rarely life-threatening, but cause considera ble distress. Make the diagnosis \200 Variable in appearance, but most commonly toxic erythema \200 \224 symmetrical, erythematous, itchy rash, trunk > extremities, lesions may be measles-like, ur ticarial, or resemble erythema multiforme Certain drugs may produce predictable eruptions: Acneiform rash with lithium \200 Bullous lesions with furosemide \200 Target lesions wi th penicillins and phenytoin \200 Psoriasis-like rash with B -blockers \200 Urticaria w ith penicillin, opiates and aspirin \200 Fixed drug eruption (round purple plaques recurr ing in the same spot) with paracetamol, laxatives, sulphonamides, and tetracyclines Toxic epidermal necrolysis is a rare, serious reaction to drugs such as non-steroidals, all opurinol, and phenytoin. The skin appears scalded, and large areas of epidermis may shear o ff causing problems with \202 uid and electrolyte balance, thermoregulation, and infectio n \200 Take a careful drug history to elicit a temporal relationship to medication administration \200\224 eg within 3 days of starting a new drug (may be as long as 3 weeks), or becoming worse every morning after a regular drug is given Stop the drug \200 Stop multiple medications one at a time (stop drugs started closest to the onset of the rash \201 rst), and watch for clinical improvement May get slightly worse before improving \200 Usually clears within 2 weeks \200 Advise the patient to avoid the drug in the future Soothe the skin \200 Emollients, cooling agents (eg calamine) and weak topical steroids may help Oral antihistamines are often given with variable success. Sedating antihistamines (eg hydroxyzine) may help sleep Treat the complications More likely if extensive and prolonged. Risks include: \200 Hypot hermia \200 Hypovolaemia \200 Secondary infection 2Consider dermatology referral if not improving after 2 weeks off the suspected drug. 148 CHAPTER 6 Drugs Proton pump inhibitors PPIs (eg omeprazole, lansoprazole) are very effective in reducing ga stric acid secretion and therefore in treating peptic ulcers and gastro-oesopha- geal re \202 ux disease (GORD). They are perceived as very safe drugs. The combination of effective ness and safety has led to them being one of the most commonly prescribed drug classes. However, PPIs are often prescribed without an appropriate indication, or are initiated appr opriately but not discontinued after a treatment course. Overall, over 50 % of PPI use is u nnecessary. Side effects \200 Common side effects are headache, nausea, diarrhea, and constipation \200 Infrequent idiosyncratic reactions include acute interstitial nephritis, erythema multiforme, pancreatitis, microscopic colitis, hyponatraemia, ad hypomagnesaemia Hydrochloric acid aids protein digestion and absorption of vitamin B 12 and calcium, and is active against pathogens. PPI use is associated with: \200 Community and hospital incide nce of CDAD and increased likelihood of recurrence Enteric bacterial infections (eg Salmonella , Campylobacter ) \200 Community- and hospita l-acquired pneumonia Long-term use is associated with higher rates of hip fracture, possibly caused by altered calcium absorption Interactions There are a few important interactions: \200 The effects of phenytoin and wa rfarin are enhanced \200 The effects of clopidogrel are reduced \200 Plasma concentrati ons of digoxin are increased slightly Appropriate prescribing \200 Always specify the indication for treatment and its intended duration \200 In GORD, always \201 rst address non-drug factors (obesity, alcohol) and consider the use of less potent acid-suppression (eg H2 antagonists such as ranitidine) Transient dyspepsia or occasional heartburn are inadequate indications for long-term PPI treatment In primary care, review the need for the drug periodically \200 In secondary care, be car eful not to extend an initial appropriate PPI prescription for prophylaxis against gastrointestinal bleeding In (con \201 rmed or possible) CDAD, consider stopping PPIs HERBAL MEDICINES 149 Herbal medicines Use of herbal supplements by older adults is common (some studies esti- ma te 30 \200\22350 % ). Most patients do not discuss this with their doctors so remember to a sk. Herbal medicines are not regulated like drugs, contain variable quantities of active in gredient and may contain impurities. Herbal medicines have adverse effects and drug interac tions (Table 6.3 ). Table 6.3 Overview of herbal medicines Name Use Adverse effects Drug interactions Garlic Hypertension High cholesterol Antiplatelet Bleeding Gastrointestinal upset Hypoglycaemia NSAIDs Antiplatelets Anticoagulants Gingko Memory problems Seizures Bleeding Headaches Dizziness Gastrointestinal upset NSAIDs Antiplatelets Anticoagulants Monoamine oxidase inhibitors (MAOIs) Trazodone Ginseng Performance enhancer Hypertension Tachycardia NSAIDs Antiplatelets Anticoagulants Hypoglycaemic agents (reduced ef \201 cacy) Glucosamine/ chondroitin Osteoarthritis Nausea Diarrhea Heartburn Cytochrome P450 drugs St John \200\231s wort Antidepressant Nausea Anticoagulants Anxiolytic Allergy Dizziness Antivirals SSRIs Statins Headache Photosensitivity Immunosuppressants Echinacea Immune stimulant Allergy Hepatitis Asthma Vertigo Valerian Anxiety Sedation CNS depressants Insomnia Saw palmetto Prostatic symptoms Constipation Finasteride Diarrhea Decreased libido Hypertension Urinary retention 150 CHAPTER 6 Drugs Breaking the rules A great deal of prescribing in geriatric practice relies on individually tai- lored assessment and pragmatic decision making. While what is described in the preced ing pages is appropriate for many, there are times when \200\230rules must be broken \200 \231 in the best interests of the individual patient. This requires careful consideration o f risks and bene \201 ts; the patient should usually be reviewed to assess the impact of t he decision. Polypharmacy can cause problems, but is sometimes appropriate \200\224 depriving patients of bene \201 cial treatments because they are old, or already on multiple other medication s, can also be wrong. In a recent study of medication changes during a geriatric admission, the total number of drugs was the same at admission and discharge, but they had often been changed. In other words, there was active evaluation of medication going on \200\224 the goal being not just to limit the number of drugs, but also to optimize and individually tai lor treatment. Where side effects are very likely, but the drug is de \201 nitely indicated, then it may be appropriate to co-prescribe something to treat the expected adverse effect, for example: \200 Steroids and bisphosphonates \200 Opiates and laxatives \200 Furosemide and a p otassium-sparing diuretic (or an ACE inhibitor) \200 Non-steroidals and a gastric protect ion agent Whilst certain disease-drug interactions are very likely, and should be avoided, others may be an acceptable risk. For example: \200 B -blockers: Are to be used with caution with asthma, yet they have such a good impact with on cardiovas cular risk reduction that these cautions are not absolute. Often the \200\230asthma \200 \231 is in fact COPD with little B -receptor reactivity, so cautious B -blockade initiated in hospital whilst monitoring the lung function may be appropriate \200 Can reduce the si gns of hypoglycaemia in diabetics, but cardiovascular disease is common in people with diabetes, and the risks of treatment are us ually outweighed by the bene \201 ts \200 In patients with peripheral vascular disease c an cause a small reduction in walking distance, but this risk is usually outweighed by the reduction in the risk of cardiac death Fludrocortisone (for postural hypotension) will worsen supine hypertension and cause ankle swelling. But if postural symptoms are severe then it may be a ppropriate to accept hypertension and associated risk Amlodipine may worsen ankle swelling in a patient with chronic venous insuf \201 ciency, b ut if this is the best way of controlling hypertension, it may be appropriate to accept a c osmetic problem 151 Chapter 7 Neurology The ageing brain and nervous system 152 Tremor 154 Neuropathic pain/neuralgia 156 HOW TO Treat neuralgia 157 Parkinson \200\231s disease: presentation 158 Parkinson \200\231s d isease: management 160 HOW TO Manage a patient with Parkinson \200\231s disease who cannot take oral medication 161 HOW TO Treat challenging symptoms in Parkinson \200\231s disease 162 Diseases masquerading as Parkinson \200\231s disease 164 Epilepsy 166 Epilepsy: drug treatm ent 168 Neuroleptic malignant syndrome 169 Motor neuron disease 170 Peripheral neuropathies 172 Subdural haematoma 174 Sleep and insomnia 176 HOW TO Use benzodiazepines for ins omnia 177 Other sleep disorders 178 152 CHAPTER 7 Neurology The ageing brain and nervous system As in other systems intrinsic ageing (occurs in all) is often hard to distinguish from extrinsic ageing mechanisms (caused by disease processes). See b \200\230Cognitive ageing \200\231, p.204 for discussion of cognitive ageing. Histological changes in the brain include: Each neuron has fewer connecting arms (dendrites) \200 Around 20 % of brain volume and we ight are lost by the age of 85 \200 There is deposition of pigment (lipofuscin) in the ce lls and oxidative damage in mitochondria The presence of senile plaques and neuro \201 brillary tangles increases with age but they are not diagnostic of dementia (Table 7.1 ) Table 7.1 Age-related changes to the nervous system Age-related change Consequence Loss of neurons (cannot be regenerated) Cerebral atrophy common on brain scans (although this does not correlate well with cognitiv e function) Decrease in brain weight (by around 20 % at age 85) Re \202 exes which have long nerve tracts, eg ankle jerks, can be diminished or lost Some neurons become demyelinated and have slowed nerve conduction speed and increased laten cy (time taken to recover before transmitting next impulse) Minor sensory loss, eg \201 ne touch/vibration sense, may be lost distally Neurotransmitter systems alter, Increased susceptibility to some neuromodulating drugs eg cholinergic receptors decrease Probably not a normal \201 nding Increasing frequency of periventricular white matter changes seen on cerebral imaging Signi \201 cance unclear \200\224 assumed to be representative of small-vessel vascular d isease but poor postmortem correlation This page intentionally left blank 154 CHAPTER 7 Neurology Tremor Tremor is more common with increasing age. It can be disabling and/or socially embar rassing. It is important to try to make a diagnosis as treat- ment is available in some cas es. Examine the patient \201 rst at rest and distracted (relaxed with arms supported on lap, count backwards from 10), then with outstretched hands and \201 nally during movement (po inting or picking up a small object). Tremors fall roughly into three categories 1. Rest tr emor \200\224 disappears on movement and is exaggerated by movement of the contralateral side of the body. Commonest cause \200\224 Parkinson \200 \231s disease. It is usually associated with increased tone 2. Postural tremor \200\224 present in outstretched limbs, may continue during action but disappears at rest. Commonest cause \200\224 benign essential tremor 3. Action tremor \200\224 exaggerated with movement. When the tremor is maximal at extreme point of movement it is called an intention tremor. Commonest cause \200\224 cerebellar dysfunction Benign essential tremor \200 The classic postural tremor of old age, worse on action (eg static at rest but spills tea from teacup) may have head nodding (titubation) or jaw/vocal tremor, le gs rarely affected. May be asymmetrical \200 About half the cases have a family history ( autosomal dominant) \200 Presents in middle age, occasionally earlier and worsens gradual ly \200 Often more socially embarrassing than physically impairing \200 Improved by alc ohol, gabapentin, primidone and B -blockers but these often unacceptable treatments in the long term. Worth considering B -blockers as \201 rst choice in treatment with coexistent hypertension Weighted wristbands can reduce tremor and improve function Parkinson \200\231s disease (see b \200\230Parkinson \200\231s disease: presentation \200\231, p.158) Cerebellar dysfuncti on The typical intention tremor is associated with ataxia. \200 Acute onset is usually va scular in older patients \200 Subacute presentations occur with tumors (including paraneo plastic syndrome), abscesses, hydrocephalus, drugs (eg anticonvulsants), hypothyroidism or toxins Chronic progressive course is seen with: Alcoholism (due to thiamine de \201 ciency \200\224 always give thiamine 100mg od orally or iv preparation if in doubt, it might be reversible) Anticonvulsant (eg phenytoin \200\224 may be irreversible if severe, commoner with high plasma levels but can occur with long-term use at therapeutic levels) Paraneoplastic syndromes (anti-cerebellar antibodies can be found, eg anti-Yo and anti-Hu f ound in cancer of ovary and bronchus) Multiple sclerosis \200 Idiopathic cerebellar atrophy \200 Many cases defy speci \201 c diagnosis. Consider multisystem atrophy TREMOR 155 Other causes of tremor (Table 7.2 ) Table 7.2 Other causes of tremor Diagnosis Recognition and characteristics Management See b \200\230Hyperthyroidism: drug treatment \200\231, p.442 Thyrotoxicosis Fine resting tremor This is actually commoner in younger patients Rigors Sudden onset coarse tremor with associated malaise and fever Diagnose and treat underlying cause Diagnose and treat underlying condition Coarse postural tremor in a sick patient with physiological disturbance Asterixis (tremor and incoordination) with hepatic, renal or respiratory failure A less dramatic, often \201 ne, tremor can occur with metabolic disturbance such as hypog lycaemia or hypocalcaemia For therapeutic drugs recommence and consider gradual controlled withdrawal at later date Drug withdrawal, Always consider when patient develops tremor confusion soon after admission eg benzodiazepines, SSRIs, barbiturates Consider treatment with, eg chlordiazepoxide and thiamine Alcohol withdrawal Always take an alcohol history. Tremor confusion develops soon after admission Drug side effects, Check serum levels are in therapeutic range. Consider a different agent eg lithium, anticonvulsants Fine tremor Rarely necessary to consider B -blockers Anxiety/stress \200\224 increased sympathomimetic activity Provide perching stools etc to avoid standing for long Fine tremor of legs on standing diminished by walking/sitting. Can palpate muscle tremor in legs. Patient feels unsteady but rarely falls Orthostatic tremor \200\224 rare, benign postural tremor of legs 156 CHAPTER 7 Neurology Neuropathic pain/neuralgia This describes pain originating from nerve damage/in \202 ammat ion. It is often very severe and debilitating and seems to be more common in older people. The pain is usually sharp/stabbing and is often intermittent being precipitated by things l ike movement and cold. Post-herpetic neuralgia \200 Severe burning and stabbing pain in a division of nerve prev iously affected by shingles Shingles and subsequent persisting neuralgia is much more common in older patients Pain may be triggered by touch or temperature change \200 May go on for years, be dif \201 cult to treat and have major impact on quality of life Prevent by starting antivirals within 72hr of rash (eg famciclovir) \200 See b \200\230H OW TO Treat neuralgia \200\231, p.157 for treatment Trigeminal neuralgia \200 Severe unilateral stabbing facial pain, usually V2, V3 rather t han V1 \200 Triggers include movement, temperature change, etc. \200 Time course \200 \224 years with relapse/remission \200 Depression and weight loss can result \200 Diffe rential diagnoses include temporal arteritis, toothache, parotitis and temporomandibular joint arthritis Consider neuroimaging especially if there are physical signs, ie sensory loss or other cranial nerve abnormality suggestive of secondary trigeminal neuralgia Bilateral trigeminal neuralgia suggests multiple sclerosis \200 See b \200\230HOW TO Treat neuralgia \200\231, p.157 for treatment Neuralgia can also occur with \200 Malignancy \200 Cord compression \200 Neuropathy NEUROPATHIC PAIN/NEURALGIA 157 HOW TO Treat neuralgia This can be very debilitating and treatment is dif \201 cult. There is often coexistent de pression, so always think of this and treat appropriately. Simple measures include \200 Distraction \200 Relaxation techniques \200 Allaying fea rs (usually about serious underlying pathology) \200 Acupuncture \200 Heat/cold treatme nt \200 Osteopathy/massage (to reduce associated muscle spasm) \200 Use of TENS machine s (transcutaneous nerve stimulation) \200 Support groups, eg M www.tna.org.uk Medications \200 Topical treatments, eg lidocaine, capsaicin \200 Traditional analgesic s (paracetamol, NSAIDs, opiates) although these are usually not very effective Anti-spasticity drugs, eg baclofen. Used especially in trigeminal neuralgia, they treat any muscle spasm that exacerbates the pain Mainstay of treatment is the neuromodulating drugs which may give superior pain control but often have important side effects. Examples include: Antidepressants with neuroadrenergic modulating abilities, eg amitriptyline, duloxetine. Start with a low dose and titrate up slowly. Eventual doses m ay be similar to those used in younger patients Anticonvulsants, eg gabapentin, pregabalin (postherpetic neuralgia) or carbamazepine, oxcar bazepine, valproate (trigeminal neuralgia). Start with a low dose and titrate up slowly The main side effects from these drugs are sedation and confusion, and reaching a therapeut ic dose may be limited by this problem. Other options \200 Nerve blocks or spinal stimulation, which can usually be accessed via a specialist pain clinic Surgery, eg nerve decompression, or treatment with heat or lasers. May provide relief but can result in scarring and numbness 158 CHAPTER 7 Neurology Parkinson \200\231s disease: presentation A common, idiopathic disease (prevalence 150/100 000) associated with inadequate dopamine neurotransmitter in brainstem. There is loss of ne urons and Lewy body formation in the substantia nigra. The clinical syndrome is distinct fr om Lewy Body dementia (See b \200\230Dementia and parkinsonism \200\231, p.214 for treatme nt) but there is overlap in some patho- logical and clinical \201 ndings leading to sugge stions they might be related conditions. Presentation The clinical diagnosis of Parkinson \200\231s disease is based on the UK Parki nson \200\231s disease brain bank criteria and should include: \200 Bradykinesia (slow to initiate and carry out movements, expressionless face, fatigability of repetitive movement) Plus at least one of the following: \200 Rigidity (cogwheeling = tremor superimposed on r igidity) \200 Tremor ( \200\230pin-rolling \200\231 of hands \200\224 worse at rest) \200 Postural instability Other clinical features: \200 Gait disorder (small steps) \200 Usually an asymmetrical disease \200 No pyramidal or cerebellar signs but re \202 exes are sometimes brisk \200 Non motor symptoms are common and should be asked about (se e b \200\230Non-motor symptoms of Parkinson \200\231s disease \200\231, p.158) Non-motor symptoms of Parkinson \200\231s disease \200 Depression (treat appropriately) \200 Psychosis (may relate to medications; avoid typical antipsychotics as they may worsen the motor features; atypicals such as quetiapine or olanzapine can be tried) Dementia and hallucinations can occur in late stages but drug side effects can cause simila r problems. If features suggest Lewy body dementia a trial of anticholinesterases may be wa rranted Sleep disturbance (treat restless legs, review medications, advise about driving if sudden onset sleep, daytime hypersomnolence may be treated with moda \201 nil) Falls (usually multifactorial, see b \200\230Assessment following a fall \200\231, p.104) \200 Autonomic features are generally late features, but common in older patients. They should be sought and actively managed: \200 Weight loss \200 Dysphagia \200 Constipation \200 Erectile dysfunction \200 Orthostatic hypotension \200 Excess ive sweating \200 Drooling PARKINSON \200\231S DISEASE: PRESENTATION 159 Investigations \200 Diagnosis is clinical, and once suspected should be reviewed by a Parkinson \200\231s disease specialist Trials of treatment may be done, with review of the diagnosis if there is no improvement, b ut single dose levodopa \200\230challenge \200\231 tests are no longer performed Brain imaging (eg CT) can be used to illustrate other conditions that may mimic Parkinson \200\231s disease (eg vascular disease) Specialist scans are becoming more widely used to assist diagnosis (eg consider 1 2 3 I-FP-CIT single photon emission computed tomography (SPECT), commonly kn own as DatSCAN \204 after the radiolabelled solution used) 160 CHAPTER 7 Neurology Parkinson \200\231s disease: management Should be overseen by a Parkinson \200\231s disease specialist clinic. Drugs It is not possible to identify a universal \201 rst-choice drug therapy for either early Parkinson \200\231s disease or for adjuvant drug therapy for later stages. Consider the short- and long-term bene \201 ts and risks of each treatment, along with lifestyle and clinical factors. Discussion with the patient is key. Initiation treatment is started with one of the following: Levodopa plus decarboxylase inhibitor (prevents peripheral breakdown of drug) (co-beneldopa/co-careldopa). Start low and titrate to symptoms \200 Dopamine ago nists (ropinirole, pergolide, cabergoline). Psychiatric side effects, postural hypotension and nausea often limit therapy MAOI (selegiline). The newer buccally absorbed preparation is better tolerated and useful i n swallowing dif \201 culties. These drugs have many interactions with antidepressants and should be used with care by a specialist Adjuvant treatment may be needed as the disease progresses. Firstly increase doses or add a second agent from the list already given then consider: \200 COMT inhibitor (entacapone) . Will smooth \202 uctuations in plasma levodopa concentrations. Give with each levodopa dose \200\224 sometimes will need levodop a dose decrease. Stains urine orange Amantadine \200\224 weak dopamine agonist which can reduce dyskinetic problems Apomorphine \200\224 subcutaneous (s/c) injections. Specialist treatment- rarely useful in older patients except to cover periods of nil by mouth Anticholinergics (benzhexol, orphenadrine) are mild anti-parkinsonian drugs rarely useful i n elderly patients due to severe psychiatric side effects. They do have a bene \201 cial e ffect on tremor and are possibly the drug of choice where tremor is more of a problem than bradykinesia.