opioids, iiRR suggests salicylates Eyes dilated or slow reacting pupil (unilateral or bilat eral), absent corneal refl ex, eyes looking in diff erent directions (III, IV, VI lesion), eyes fi xed: doll \200\231s head movements (not drifting back to forwards gaze when neck ro tated) Swallow water not swallowed spontaneously/no gag refl ex Respiration apnoeas, gaspin g, irregular or Cheyne \200\223Stokes breathing (alternating rapid breathing and apnoeas) B ody increased tone and upgoing plantars unilaterally/ bilaterally/crossed Facial asymmetry, asymmetrical tone and plantar responses Brainstem dysfunction Lateralising (cerebral dysfunction) Meningism Neck stiff ness, photophobia, Kernig \200\231s sign, Brudzinski \200\231s sign, straight le g raise (b p132) _OHFP.indb 339 _OHFP.indb 339 30/05/2014 16:18 30/05/2014 16:18 340 CHAPTER 11 Neurology and psychiatry Coma and reduced GCS Think about \200 No focal neurology dO2, iCO2, hypotension, metabolic (i/dglucose, Na+, C a2+, K+; acidosis, alkalosis, renal failure, liver failure), overdose (alcohol, opioids, tr icyclics, benzodiazepines), epilepsy/post-ictal, hypothermia, pyrexia, hypothyroid, maligna nt hypertension Brainstem dysfunction or lateralising signs CVA, tumor, abscess, haematoma, hypoglycaemia o r rarely other metabolic abnormalities Meningism meningitis, encephalitis, subarachnoid hemorrhage. Ask about (notes, relatives, n urses) speed of onset, headache, chest pain, palpitations, vomiting, seizures, weight loss; PMH cardiac, respira- tory, DM, kidney, liver, psychiatric, stroke/TIA, seizures; DH elici t past medical history from medications, consider the possibility of overdose; SH alcohol, recreational drugs (overdose or withdrawal). Obs GCS (Table 11.2), temp, BP, HR, O2 sats, O2 requirements, RR, pupil size. Neuro obs GCS, limb movements, pupil size and reactivity, HR, BP, RR, temp. Look for respiration rate, depth, distress, added sounds, air entry on both sides; pulse ra te and rhythm; abdomen rigidity, pulsatile mass, organomegaly; neuro pupil responses, papil loedema (late sign), limb tone, plantar refl exes; skin rashes, injection marks or trauma. Investigations blds FBC, U+E, LFT, Ca2+, glucose, cardiac markers, CRP, clotting, bld cultu res, toxicology screen (paracetamol, salicylate, alcohol); ABG pH, dO2 or diCO2; ECG arrhyt hmias; CXR evidence of aspiration; CT if the patient has focal neurology or there is no cle ar diagnosis then an urgent CT head is required, the patient may need to be intubated fi rs t; LP after a CT scan if CT normal. Table 11.2 GCS scoring (3/15 minimum) Eyes Open spontaneously 4 Motor Obeys commands 3 2 1 6 Localizes pain 5 Flexes/withdraws to pain 4 3 Abnormal fl exion to pain 2 Extension to pa in 1 No movement Open to command Open to pain No response Voice Talking and orientated 5 4 Confused/disorientated Inappropriate words 3 Incomprehensible sounds 2 1 No vocalizatio ns Originally described in 1974 as a 14-point scale (omitting \200\230abnormal fl exion \200 \231) by neurosurgeons at the University of Glasgow for use in patients with head injuries, this revised scale is now widely used in acute medicine and trauma. OHFP.indb 340 OHFP.indb 340 30/05/2014 16:18 30/05/2014 16:18 341 ACUTE CONFUSION Acute confusion 1 Delirium or acute confusional state is a common but easily missed diag- n osis associated with increased morbidity and mortality. Delirium can aff ect any patient bu t is especially common in the hospitalized elderly, where it may be misdiagnosed as dementi a (with which it may co-exist). Unlike dementia, delirium is often fl uctuating, worse at c ertain times of day.2 uctuat g, wo se at ce ta t es o ay. e u CAM: Confusion assessment met hod3 This validated aid to the recognition of delirium requires the presence of: \200 Acu te onset + fl uctuating course and \200 Inattention (easily distractible) Both of the abo ve must be present, together with either of: or s o te Disorganized thinking Altered level of consciousness Think about emergencies dO2, iCO2, MI, CVA, intracranial bleed, men- ingitis, encephalitis; common sepsis, metabolic (dglucose, dNa+), drug tox- icity (opioids, benzodiazepines, post -GA), heart failure, head injury, alcohol withdrawal or intoxication, post-ictal, urinary r etention, constipation, pain. Ask about use direct questions to assess eg for pain; further history from the ward staff , relatives, notes or residential/nursing home: speed of onset , chest pain, cough, sputum, dysuria, frequency, incontinence, head injury, headache, photo phobia, vomiting, dizziness; PMH DM, heart, lung, liver or kidney problems, epilepsy, demen tia, psychiatric illness; DH ben- zodiazepines, antidepressants, opioids, steroids, NSAIDs, antiparkinsonian drugs; SH alcohol, recreational drugs, baseline mobility and state. Obs G CS (Table 11.2), temp, HR, BP, RR, O2 sats. Look for respiration rate, depth, added sounds, cyanosis; pulse rate and rhythm; abdomen rigidity, palpable bladder; PR fecal impaction; n euro signs of head injury, pupil responses, neck stiff ness, photophobia, focal neurology, plantar responses; AMT score (see Table 11.3). Investigations urine dipstick, M,C+S; blds F BC, U+E, LFT, CRP, glucose, Ca2+, consider cardiac markers, blood cultures, amylase, TFT, B 12, folate; ABG dO2 diCO2; ECG arrhythmias; CXR infection or aspiration; CT if focal neur ology, head injury or non-resolving confusion; LP if CT normal. Table 11.3 Abbreviated Mental Test (AMT) score ( \211 8 is normal for an elderly patient) 1 Age 1 Date of birth Current year 1 Time (nearest hour) 1 1 Name of hospital Recognize two people (eg Dr, nurse) Year World War Two ended (1945) Who is on the throne (E lizabeth II) Recall address: \200\23042 West Street \200\231 Count backwards from 20 to 1 1 1 1 1 1 Management \200 Nurse in a quiet, appropriately lit environment with close, supportive observation (relatives, \200\230special \200\231 nurse); avoid restraints Investigate and treat the cause; pain and infection are the most common \200 Sedate only if patient or staff safety threatened; use oral route where possible (eg haloperidol 0.5 \200\2231mg PO/1 \200\2232mg IM every 1 \200\2232h, max 5mg/24h; if PMH Lewy body dementia, alcohol excess or Parkinson \200\231s, lorazepam 0.5 \200\2231mg PO/IM every 1 \200\2232h, max 3mg/24h). 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG103 2 Typically \200\230out- of-hours \200\231, when you may be asked to review whilst on-call. 3 Inouye, S.K. et al. An n Intern Med. 1990 113:941 (requires subscription) _OHFP.indb 341 _OHFP.indb 341 30/05/2014 16:18 30/05/2014 16:18 342 CHAPTER 11 Neurology and psychiatry Dementia 1 Progressive global cognitive impairment with normal consciousness. Worrying features rapid progression, <65yr. Think about common Alzheimer \200\231s, Lewy body disease, frontotemporal dementia (Pick \200\231s), vascular dementia, Parkinson \200\231s (late), normal pressure hydrocephalus, d epression (pseudodementia), chronic subdural haema- toma, Korsakoff \200\231s syndrome; ra re HIV, CJD, syphilis, space-occupying lesions, hypothyroid, B12 defi ciency, malnutrition. Ask about age of onset, progression, memory (short and long term), personality, thinking, planning, judgment, language, visuospatial skills, concentration, social behavior, confusio n, wandering, falls, head injury, tremor, mood, sleep quality, delusions, hallucinations, h earing, sight; PMH seizures, CVA/TIA; DH regular medications, sleeping tablets, anticholine rgics; FH dementia, neurological problems; SH eff ect on work, relationships and social abi lities; independence with activities of daily living (ADLs \200\223 food, cleaning, washin g, dressing, toilet); ability to manage fi nances; alcohol intake; try to build a picture o f the domestic environment: Who is at home and what local support is available? Obs GCS, HR, BP, glucose. Look for Mini-Mental State Examination (b p343), Abbreviated Ment al Test score (b p341); full systems exam with careful neurological exam including general appearance, tremor, gait, dysphasia, cog-wheeling. Investigations blds FBC, ESR, U+E, LFT, Ca2+, TFT, B12, folate, consider HIV, VDRL/TPHA; imaging, CXR, CT/MRI brain; ECG; LP; EEG. Management The aim of initial investigations is to rule out and treat any reversible causes ; refer to a neurologist/psychogeriatrician for specialist diagnosis and management; use an MDT approach to ensure the patient has appropriate accommodation and support with ADLs. Support organizations High-quality advice and access to support for dementia suff erers and their carers is available from a number of organizations, including: \200 Dementia UK (0 845 257 9406 (cid:27)www.dementiauk.org) \200 Alzheimer s Society (0300 222 1122 (cid:27) www.alzheimers.org.uk) [for England, Wales and Northern Ireland] or Alzheimer s Scotland (0808 808 3000 (cid:27)ww w.alzscot.org) [for those in Scotland] \200 Carers Direct (0808 802 0202 (cid:27)www.nhs. uk/carersdirect) for telephone and online support and advice for carers Age UK (0800 169 6565 (cid:27)www.ageuk.org.uk) for a wide range of advice and services in support of ageing people 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG42 OHFP.indb 342 OHFP.indb 342 30/05/2014 16:18 30/05/2014 16:18 343 DEMENTIA Common types of dementia Alzheimer \200\231s slowly progressive loss of memory, with later loss of language, executive or visuospatial functions; anticholinesterases (eg donepezil) m ay benefi t in moderate disease. Vascular impairment of memory and at least one other cogni tive domain in the presence of vascular risk factors neuroimaging evidence of ischaemia; often co-exists with Alzheimer \200\231s. Lewy body early loss of executive function, with hallucinations (espe- cially visual) and fl uctuating levels of consciousness; memory loss is a later feature. Frontotemporal prominent and early language loss loss of social funct ioning/disinhibition; may present in younger age group. Some potentially reversible causes of dementia Sub-dural haematoma dementia focal neurolo gy (eg limb weak- ness); more common in elderly, atrophic brains; often history of trauma; characteristic CT appearances; evacuate. Normal pressure hydrocephalus dementia, gait distu rbance and urinary incontinence with hydrocephalus on CT and normal CSF opening pressure; i diopathic (50%) or may occur after meningitis, trauma or subarachnoid hemorrhage; ventricul o-peritoneal shunt may improve symptoms. Korsakoff \200\231s syndrome amnesia and confabul ation seen in thiamine defi ciency (eg alcoholism); may show very slow and limited improve- ment with thiamine replacement. Mini-Mental State Examination (MMSE)1 Since its publication in 1975, the MMSE has become a widely used test of cognitive function and is commonly used in screening for, and assessing progression of dementia. In 2001, the authors transferred reproduction and distribution ri ghts to a commercial organization which has since aggressively asserted copyright claims. N onetheless, the full test remains widely available to use in most hospitals. The test consi sts of 30 questions which together test various compo- nents of a patient \200\231s mental state: \200 orientation (in time, place and person) \200 registration (ability to liste n and recite, to obey commands) \200 attention and arithmetic (counting backwards) \200 recall (reciting a list of objects) \200 language (naming objects, reciting an address, etc) \200 executive function (copying a drawing) The maximum score in the MMSE is 30, tho ugh \211 28 is regarded as \200\230normal \200\231. Scores of 24 \200\22327 are borderlin e and <24 suggests dementia. Results are unreliable if the patient is delirious, has a sens ory impairment, aff ective disorder or has not been taught to read and write in English. An abbreviated (10-point) version is often used (b p341) and correlates well with MMSE for th ose with very high or low scores; in the interme- diate range and for tracking changes, MMS E is a more reliable test; there are also numerous other, less widely used tests of cogniti ve function.2 1 Folstein, M.F. et al. J Psychiatr Res 1975 12:189 (requires subscription). 2 Holsinger, T. et al. JAMA 2007 297:2391 (available free online at (cid:27)jama.ama-assn.o rg/cgi/ content/full/297/21/2391) _OHFP.indb 343 _OHFP.indb 343 30/05/2014 16:18 30/05/2014 16:18 344 CHAPTER 11 Neurology and psychiatry Adult seizures emergency Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM If no palpable pulse \200\223 CALL ARREST TEAM Airway Breathing Circulation If GCS \211 8 \200\223 CALL anesthetist Disability 3Call for senior help if seizure >5min. All timings are from the start of the fi rst fi t; the clock only restarts once the patient has been fi t-free >30mins. 0 \200\2235min \200 Start timing; this is very important and easy to forget \200 15l/mi n O2 in all patients \200 Keep patient safe and put into recovery position if possible \200 Monitor HR, O2 sats, BP, cardiac trace, temp \200 Venous access (after 3 \200\2234m in). Take bloods: FBC, U+E, LFT, Ca2+, glucose, bld cultures, anticonvulsant levels \200 Check GLUCOSE: if <3.5mmol/l give 100ml of 20% glucose STAT. 5 \200\22320min \200 Call for senior help and attach a cardiac monitor \200 Consider an airway adjunct but do not force teeth apart \200 If IV access: lorazepam 4mg IV over 2min, repeat at 10min if no eff ect If no IV access: diazepam 10mg PR, repeat every 10min if no eff ect up to 30mg total Ask ward staff about history/check notes \200 If alcoholism/malnourished give Pabrinex 2 pairs IV over 10min if not already given this admission. 20 \200\22340min \200 Call for anesthetist and senior help \200 If not taking phenytoin : phenytoin 20mg/kg IV at <50mg/min \200 If taking phenytoin: phenobarbital 10mg/kg IV ov er 10min (max 1g) \200 Monitor ECG, BP and temp. >40min \200 Thiopental or propofol on ICU/HDU \200 Transfer to ICU for general anesthetic and EEG monitoring. Life-threatening causes Hypoxia/cardiac disease \200 Hypoglycaemia \200 Metabolic (dCa2+, idNa+) \200 Trauma Meningitis, encephalitis, malaria \200 iICP and CVA \200 Drug overdose \200 Hypertens ion/eclampsia (pregnancy) OHFP.indb 344 OHFP.indb 344 30/05/2014 16:18 30/05/2014 16:18 345 pediatric SEIZURES EMERGENCY Pediatric seizures emergency Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM Airway Breathing If no palpable pulse \200\223 CALL ARREST TEAM If GCS \211 8 \200\223 CALL anesthetist Circulation Disability 3Call for senior help in all children having a seizure. All timings are from the start of t he fi rst fi t; the clock only restarts with a fi t-free period >30mins. Step 1 \200 Start timing; this is very important and easy to forget \200 Maintain airwa y, assess ABC, check pupil size, posture, neck stiff ness, fontanelle, temp and for rashes 15l/min O2 in all patients \200 Check GLUCOSE: if <3.5mmol/l give 2ml/kg of 10% glucose S TAT: \200 take 10ml of clotted blood and one fl uoride bottle (b p520) prior to giving glucose, but don \200\231t let this delay treatment Keep patient safe, be alert for vomit occluding the airway \200 Monitor HR, O2 sats, BP, cardiac trace, temp \200 Venous access, take bloods: FBC, U+E, LFT, CRP, Ca2+, Mg2+, glucose, bld cultures, anticonvulsant levels (if on anticonvulsants), venous blood gas If IV access: further lorazepam 0.1mg/kg IV (max 4mg) \200 If no IV access: diazepam 0.5m g/kg PR (max 10mg) \200 Ask parents or ward staff about history/check notes. Step 2 (10mi n after either lorazepam/diazepam) \200 If IV access: further lorazepam 0.1mg/kg IV (max 4mg) \200 If no IV access: paraldehyde 0.4ml/kg PR with 0.4ml/kg olive oil or 0.8ml/kg of a pre-prepared 50:50 solution (max 20ml of mixture). Step 3 (10min after either lorazepam/paraldehyde) \200 Call for anesthetist and senior he lp \200 Paraldehyde 0.4ml/kg PR as above unless already given \200 If not on phenytoin: phenytoin 20mg/kg IV/IO at <50mg/min \200 If on phenytoin: phenobarbital 20mg/kg IV/IO o ver 20min. Step 4 (20min after either phenytoin/phenobarbital) \200 Rapid sequence intuba tion \200 Consider mannitol, pyridoxine, paracetamol, diclofenac. Life-threatening causes Meningitis, encephalitis, malaria \200 Hypoglycaemia \200 Metabolic (dCa2+, idNa+) \200 Trauma/non-accidental injury Hypoxia \200 iICP and CVA \200 Drug overdose \200 Hypertension _OHFP.indb 345 _OHFP.indb 345 30/05/2014 16:18 30/05/2014 16:18 346 CHAPTER 11 Neurology and psychiatry Seizures Worrying features preceding headache or head injury, duration >5min, prolonged post-ictal p hase, adult onset, recent depression (overdose). Think about life-threatening see box (b p344); most likely idiopathic (>50%), epilepsy, alc ohol withdrawal, hypoglycaemia, hypoxia, trauma; other kidney or liver failure, pseudoseizu res, overdose (tricyclics, phe- nothiazines, amphetamines); non-seizure brief limb jerking during a faint, rigors, syncope, arrhythmias. See Table 11.4. Ask about get a detailed description of the fi t from anyone ante- who witnessed cedent sob ; pmh previous seizures, dm, alcoholism, cardiac, respiratory, renal or hepatic disease, pr egnant; DH anticonvulsants, hypoglycaemics; SH alcohol intake, last drink, recreational dru gs, recent travel; FH epilepsy. the trauma, episode (see box); headache, head chest pain, palpitations, Obs GCS, temp, glucose (recheck), BP, O2 sats. Look for sweating, tremor, head injury, tong ue biting, neck stiff ness, papilloedema, focal neurology, urinary or fecal incontinence, p reg- nancy, infection, limb trauma (eg posterior dislocation of shoulder). Investigations b lds FBC, U+E, LFT, glucose, Ca2+, Mg2+, blood cultures, anticonvulsant levels; ABG if hypox ia or metabolic upset suspected; urine consider drug screen, B-hCG if pre-menopausal 5; ECG to exclude dys- rhythmia; CT may show a focal lesion, iICP, hemorrhage or infarction, perf orm as urgent if the patient has a persistent GCS <15 post-fi t, focal neu- rology or if th e seizure was <4d post-trauma; MRI is the neuroimaging of choice in suspected epilepsy; LP if meningitis or encephalitis suspected; EEG may help to exclude encephalitis or as out-pat ient investigation for epilepsy. Treatment Stop the seizure using the treatment outlined on b p344. Correct any metabolic upset (glucose, Mg2+, Ca2+, Na+) and exclude life-threatenin g causes whilst trying to establish the cause. Secure airway if still fi tting or GCS \211 8. Describing a seizure If witnessing a seizure, try to document: \200 Onset position, activ ity, any warning, starting in one limb or all over, presence of tonic phase (arched back, muscle spasm) During loss of consciousness, limb movements, eye movements, jaw and lip movements, breathi ng, peripheral or central cyanosis, incontinence (urinary and fecal), duration, HR and rhyt hm Afterwards tongue trauma, sleepy, limb weakness (Todd \200\231s paresis, b p348). OHFP.indb 346 OHFP.indb 346 30/05/2014 16:18 30/05/2014 16:18 347 SEIZURES Table 11.4 Common causes of transient loss of consciousness History Known epilepsy, may have aura, post-ictal confusion/weakness Examination Often normal, may have tongue or limb trauma Investigations Often normal, may have focal lesion or metabolic cause iMCV and GGT; may hav e a mild anemia Normal investigations Epileptic seizure (b p348) Anxious, sweating, tachycardic, tremor liver disease Responsive to pain, normal respirati on, no injuries iWBC, N \230 or Febrile, source of L \230 and CRP, +ve infection (eg UTI, u rine dipstick pneumonia), no injury iBP, palpable uterus Proteinuria, Alcohol withdrawal (b p348) Pseudo- seizures/ psychogenic Rigors Usually >50units/wk alcohol consumption, last drink >24h ago Unusual features, short durati on, memory of event Feels cold/hot, no LOC, coarse shaking, infection symptoms Pregnant, ma y be unaware Eclampsia (b p504) fetal heart on Doppler Arrhythmia or heart block on ECG, 24h ECG and BP monitoring HLA typi ng, sleep studies Evidence of cardiac disease, injury following fall, irregular/absent pulse during attack Of ten normal; loss of postural muscle tone and tendon refl exes during attacks Bradycardia an d hypotension during episode, GCS 15/15 within min, no focal neurology Transient arrhythmia/ Stokes \200\223 Adams Palpitations, pale, sudden LOC limb jerking; rapid recovery with fl ushing Narcolepsy Excessive daytime sleepiness, collapse, sleep paralysis hallucinations Feels light-headed hot, then colla pse while standing, fi ne limb jerking, urinary incontinence, rapid recovery, no post- ictal phase postural drop (systolic drop of 20mmHg or more) Vasovagal syncope (b p260) Assessing a \200\230 \201 rst \201 t \200\231 History Detailed account from a fi rst-ha nd witness. 3 \210\222, clotting, medi- Investigations FBC, U+E, LFT, glucose, Ca2+, Mg2+, PO4 cation levels, urine and serum toxicology screen (including paracetamol and salicylate) ; CT to exclude structural causes (non-urgent, unless recent trauma or altered neurology); consider LP after CT only if infection suspected; MRI is the neurologists \200\231 imaging of choice in suspected epilepsy, but can be arranged from their clinic. Management Admit on ly if GCS<15 or drowsy; discuss with senior doctor regarding suspicion of seizures and need to advise to stop driving (see b p605, 1yr ban); do not start antiepileptic medication \200\223 this decision should be made by a neurologist in an urgent out-patient clinic ( \200\230fi rst fi t \200\231 clinic). Causes of seizures elsewhere in this book b p360 b p323 b p388 Hypertensive emergency b p262 b p260 Hypoxia Meningitis/encephalitis b p360 b p504 Raised ICP Hypoglycaemia Hypocalcaemia Hyper/hyponatraemia b p387/386 Eclampsia _OHFP.indb 347 _OHFP.indb 347 30/05/2014 16:18 30/05/2014 16:18 348 CHAPTER 11 Neurology and psychiatry Epilepsy1 (OHCM9 b p494) The abnormal, unprovoked discharge of a group of neurons results i n an epileptic seizure; epilepsy is the recurrence of \211 2 such seizures. Symptoms depen d upon where the misfi ring neurons are located. Seizures may be classifi ed based upon a c areful history into: \200 Partial seizures start in a focal area of the brain giving, eg stereotyped motor, sensory, or autonomic symptoms; further subcategorised as: \200 simple partial seizure with preserved consciousness \200 complex partial seizure with altered c onsciousness, eg temporal lobe epilepsy (altered mood, hallucinations, stereotyped movement s) \200 secondary generalized seizures start focally with a partial seizure, and evolve t o the widespread discharge of generalized seizures \200 Generalized seizures involve both cerebral hemispheres and include: \200 tonic \200\223clonic with LOC and initial muscle spasm of whole body (tonic) followed by jerking phase (clonic) absence sudden stopping of activity with staring or eye rolling, lasts <45s, most common in children. Signs dGCS, tongue trauma, limb weakness, incontinence, Todd \200\231s paresis (transient w eakness following a seizure; mimics a TIA). Investigations often normal; MRI and EEG ( pro vocation) may help with the diagnosis and seizure classifi cation. Treatment decisions rega rding use, titration and cessation of antiepileptic medications should be taken by an epile psy specialist, and involve the patient. When treating a patient with epilepsy, be aware th at certain drugs can lower seizure thresholds (eg fl uoroquinolones, cephalosporins, penici llins, pethidine, tricyclics, clozapine); seek advice from a pharmacist. Always ensure pati ents are able to take their antiepileptic medication (eg consider NG or IV preparations if NBM). Alcohol withdrawal (OHAM3 b p414) Symptoms 12 \200\22336h post-alcohol: anxiety, shak ing, sweating, vomiting, tonic- clonic seizures; 3 \200\2234d post-alcohol delirium tremens may develop: coarse tremor, confusion, delusions, hallucinations (untreated mortality 15%) . Signs hypertension, tachycardia, pale, sweaty, tremor, hypoglycaemia; delirium tremens: p yrexia. Investigations blds may have dMg2+, dPO4 Treatment monitor patients with a signifi cant alcohol history for with- drawal; prescribe a reducing dose of chlordiazepoxide (b p19 3); correct electrolyte abnormalities; give vitamin replacements PO (thiamine 25mg/24h and vitamin B (compound strong) one tablet/24h) or IV (Pabrinex 2 pairs/8h IV for 5d; this is a high-potency combination of B and C vitamins that may sometimes cause anaphylaxis). Moni tor BP and blood glucose. Withdrawal seizures are usually self-limiting, treat as b p344 if required. Complications seizures, coma, encephalopathy, hypoglycaemia. 3 \210\222 or durea. Post-traumatic seizures Seen in more severe traumatic brain injury, where antiepileptic dru gs are often used prophylactically. Arrange an urgent CT scan if not already done; if haema toma seen (b p438), contact a neurosurgeon, otherwise hourly neuro obs and reassess if dGCS . 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG137 OHFP.indb 348 OHFP.indb 348 30/05/2014 16:18 30/05/2014 16:18 349 NEURODEGENERATIVE DISORDERS Neurodegenerative disorders Parkinson \200\231s disease1 (OHCM9 b p498) Common neurological disorder (aff ects 71% of >60yr). Cardinal features include resting tremor, rigidity and b radykinesia. Symptoms and signs coarse resting tremor ( \200\230pill rolling \200\231, usua lly unilateral at onset); rigidity ( \200\230cog-wheeling \200\231); stumbling, festinant g ait; small hand- writing, depression, speech and swallowing problems; sensation normal. Inv estigations clinical diagnosis; single photon emission CT (SPECT) if diagnostic uncertainty ; exclude other causes of similar symptoms of \200\230Parkinsonism \200\231, eg drug induc ed (haloperidol). Treatment Antiparkinsonian medications should be initiated and titrated b y a specialist. Levodopa given together with a peripheral dopa-decarboxylase inhibitor (eg carbidopa) enhances dopaminergic transmission. Eff ectiveness reduces after some years, so start only when symptoms interfere with life. Problematic \200\230on-off \200\231 and \200\230end-of-dose \200\231 phenomena may require addition of a monoamine-oxidase-B inhibi tor (eg selegiline) or a COMT-inhibitor (eg tolcapone). Dopamine agonists (eg ropinirole) g ive slightly less eff ective symptom control but have fewer side eff ects so may be preferr ed in early therapy. Medications need to be given at precise times which may require altera tion of standard in-patient drug charts. Complications depression, dementia (late stage): P arkinson \200\231s disease may have pathological overlap with Lewy body dementia (b p343) w ith movement and cognitive dysfunction coming at contrasting stages in each disease. Parkin son \200\231s-plus syndromes share some features of Parkinson \200\231s (eg multi- system a trophy: Parkinson \200\231s plus autonomic and cerebellar dysfunction; progressive supranuc lear palsy: Parkinson \200\231s plus impaired upwards gaze). These tend to be refractory to standard therapy. Motor neuron disease2 Degenerative disease aff ecting upper and lower mo tor neurons. Symptoms and signs slowly progressive painless weakness, with mixed UMN and LM N features (b p353) eg spasticity, fasciculations; later speech and swallowing diffi cultie s leading to aspiration. Investigations EMG fi brillation and fasciculations. Treatment mos tly symptomatic, life expectancy is usually 3 \200\2235yr. Complications aspiration pneumon ia, respiratory failure, spasticity. Huntington \200\231s disease Incurable inherited (auto somal dominant) disorder characterized by involuntary limb movements (chorea), dementia and behavioral distur- bance (depression, psychoses). Onset at 30 \200\22350yr. Friedreich \200\231s ataxia Inherited (autosomal recessive) disorder characterized by progr essive limb and gait ataxia, dysarthria, loss of proprioception, absent tendon refl exes in the legs, and extensor plantar responses. Inability to walk occurs 715 years after disease onset. May also develop heart failure and DM. Supportive management. 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG35 2 Resources for patients, carers and doctors at (cid:27)www.mndassociation.org _OHFP.indb 349 _OHFP.indb 349 30/05/2014 16:18 30/05/2014 16:18 350 CHAPTER 11 Neurology and psychiatry Stroke/CVA/TIA emergency Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM If no palpable pulse \200\223 CALL ARREST TEAM If GCS \211 8 \200\223 CALL anesthetist Airway Breathing Circulation Disability 3Call for senior help early. Pt may need immediate transfer to Hyperacute Stroke Unit (HASU ). If GCS is reduced see b p338. \200 15l/min O2 if SOB or sats <94% \200 Check blood g lucose; treat if too low (b p322) or high (b p324) \200 Check temp; treat if too low (bla nkets) or high (IV/PR paracetamol) \200 Monitor O2 sats, RR, HR, cardiac trace, temp and BP \200 Venous access, take bloods: FBC, ESR, U+E, LFT, lipids, glucose, cardiac markers, clotting, G+S NBM and start IV \202 uids for hydration (eg 0.9% saline at 100ml/h) \200 ECG looking f or atrial fi brillation or arrhythmia \200 Take a focused history particularly: when did the symptoms start (get an exact time)? \200 are symptoms worsening, static or i mproving? \200 intracranial pathology, clotting problems, bleeding (eg GI/ PV), pregnancy, recent trauma/invasive procedures/surgery/ thrombolysis Examine patient: RS, CVS, abdo and neuro exam: document exact neurological defi cits Request urgent CT scan \200 Consider thrombolysis (see box) OR aspirin 300mg PO STAT afte r CT. \200 Reassess, starting with A, B, C \200 Consider thrombolysis with t-PA in CVA if: \200 Age <80: \211 4.5 hours from start of sy mptoms (and possibly even if 4.5-6h from start of symptoms though benefi ts less) Age \211 80: \211 3 hours from start of symptoms \200 Non-haemorrhagic stroke (excluded by CT) \200 Signifi cant symptoms and not improving. Contraindications as for cardiac th rombolysis b p536. Key diff erentials Hypo/hyperglycaemia b p323 Other intracranial pathology b p353 b p346 Encephalitis/meningit is b p360 Seizure/Todd \200\231s paresis b p493 Severe liver/renal failure b p313/373 b p355 Hypertensive Overdose b p265 Bell \200\231s palsy encephalopathy OHFP.indb 350 OHFP.indb 350 30/05/2014 16:18 30/05/2014 16:18 351 STROKE Stroke 1 Neurological disability due to sudden loss of perfusion of an area of brain. Cause s ischaemia (85%, eg AF, carotid stenosis) or hemorrhage (15%). Symptoms sudden onset focal neurology though onset can be stuttering. Signs Check for irregular heartbeat and carotid bruit. The Bamford stroke classifi cation (see Table 11.5) allows easy recognition of the a rea of brain aff ected, as well as prognostication. Posterior circulation strokes (POCS) af f ect the territory of the vertebrobasilar artery (occipital lobes, brainstem and cerebellu m). Anterior circulation strokes involve the internal carotid artery territory, which suppl ies all the rest of brain. These are further subcategorised as Total anterior circulation s troke (TACS), Partial anterior circulation stroke (PACS), and Lacunar stroke (LACS) Table 11.5 Bamford stroke classi \201 cation2 TACS All of: Motor/sensory defi cit in \211 2 of face, arm, leg Homonymous hemianopia3 Higher cortical dysfunction4 2 out of 3 of TACS criteria met Higher cortical dysfunction alone Isolated motor defi cit not meeting LACS cr iteria Motor and/or sensory defi cit aff ecting \211 2 of face, arm, leg No higher cortica l dysfunction or hemianopia Ipsilateral cranial nerve palsy + contralateral motor/sensory d efi cit Bilateral motor/sensory defi cit Disordered conjugate eye movement Cerebellar dysfu nction Isolated hemianopia or cortical blindness PACS Either: or: or: LACS POCS Any of: 2 Bamford, J. et al. Lancet 1991 337:1521 (subscription required). 3 Loss of vision on the same side in both eyes (b p133). 4 Includes dysphasia, visuospatial problems, dGCS. Prognosis LACS, PACS, and POCS have a similar prognosis with 15% mortality by 1yr while 60% live independently; TACS carries a 1yr mortality of 60% with only 5% living independently. Investigations blds FBC, U+E, LFT, glucose, lipids, clotting; ECG; CXR; CT head: urgent if within thrombolysis window, GCS persistently low, on oral anticoagulants/known bleeding di sorder, severe headache at onset of stroke or evidence of iICP; otherwise within 24h. Anter ior circulation strokes also require echo, carotid Doppler and 24h ECG. Treatment see emerg ency treatment b p350; if the patient is a candidate for thrombolysis,5 move fast to ensure timely treatment. Otherwise, aspirin 300mg/24h PO/PR for 14d (provided no hemorrhage on CT ). Assess safety of swallow (b p352); if concerns, keep NBM+IV fl uids and request SALT ass essment. Monitor BP, but do not try to lower BP without discussing with a senior (b p264). Do not use LMWH in acute setting with haemor- rhagic or ischaemic strokes (risk of haemorrh agic transformation). Do not prescribe TEDS (high risk of pressure ulcers). Admit to stroke ward for early mobilization and rehabilitation with multidisciplinary team. Complications aspiration pneumonia, dependent lifestyle, further CVA. 1 NICE guidelines available at (cid :27)guidance.nice.org.uk/CG68 5 See Consider thrombolysis box and resources from the inte rnational stroke trial collabora- tors, available free at (cid:27)www.dcn.ed.ac.uk/ist3 _OHFP.indb 351 _OHFP.indb 351 30/05/2014 16:18 30/05/2014 16:18 352 CHAPTER 11 Neurology and psychiatry Transient ischaemic attack (TIA) A transient episode of neurological dysfunction caused by focal brain ischaemia without infarction. Symptoms typically last less than an hour, but pr olonged episodes can occur. Symptoms/signs as for stroke but resolve completely (though cla ssical defi nitions of TIA describe resolution within 24h, there is no precise time cutoff to distinguish ischaemia from infarction); note that a transient loss of consciousness, or \200\230dizzy turns \200\231 are unlikely to represent a TIA. Management if <3h since symp toms began see b p350; use ABCD2 score to estimate risk of stroke (see Table 11.6) start as pirin 300mg/24h PO. Table 11.6 ABCD2 score to calculate 7d stroke risk1 Age BP Clinical features Unilateral wea kness 1 point \211 60yr Systolic >140mmHg and/or diastolic \211 90mmHg 1 point 2 points 1 point 0 points 2 points 1 point 0 points 1 point Speech disturbance without weakness Other signs \211 60min 10 \200\22359min <10min Yes 7d risk 1.2% 5.9% 11.7% Duration Diabetes Total Score 0 \200\2233 4 \200\2235 6 \200\2237 Management Urgent out-patient \200\230TIA clinic \200\231 follow-up (1wk) Discuss with str oke physician \200\223 likely to need admission for urgent investigation 1 Johnston, S.C. et al. Lancet 2007 369:283 (subscription required). CVA prevention the risk of further events after TIA or stroke can be reduced with close att ention to risk factors. Medical management includes control of BP, cholesterol, and glycaem ia. Antiplatelet therapy options include clopidogrel 75mg/24h PO, aspirin 75mg/24h and dipy ridamole MR 200mg/12h PO: Current health-economic modeling favors the use of clopidogrel fo r those who have had a stroke, and aspirin/dipyridamole combination therapy after a TIA.2 E ncourage smoking cessation, healthy diet and moderate exercise. Carotid endarterectomy shou ld be considered within 2wk if symptomatic carotid stenosis >70%. Safe to swallow? For any patient with dGCS or a suspected neurological disability, perform a simple test of a patient \200\231s safety to swallow by watching the patient attempt to d rink 30ml of water while seated in an upright position. Monitor for: \200 Delayed swallow ing (>2s to initiate swallow) \200 Drooling \200 Cough during or within 1min of swallow ing \200 Dysphonia/ \200\230wet voice \200\231 after swallowing. If any of these features are present, keep NBM+IV fl uids and request a SALT assessment. 2 NICE interpretation of study data; see (cid:27)guidance.nice.org.uk/TA210 OHFP.indb 352 OHFP.indb 352 30/05/2014 16:18 30/05/2014 16:18 353 FOCAL NEUROLOGY Focal neurology Worrying features dHR, i/dBP, dGCS, severe headache, pyrexia, neck stiff ness, photophobia, vomiting, papilloedema. Think about try to establish an anatomical pattern to abnormalities that will narrow the di ff erential diagnosis (see Table 11.7 b p354). Ask about motor problems (weakness, gait disturbance); sensory disturbance (tingling, pain, numbness); features of cerebellar disease (clumsiness, dysphasia, gait disturbance); sympt oms of cranial nerve and cerebrum involvement (double vision, blurred vision, vertigo, hear ing loss, dysphasia, facial droop); establish speed of onset and signs of underlying diseas e (weight loss, fever, cough, photophobia, neck stiff ness, rashes, behavioral change) or i ICP (headache, nausea, morning vomiting); PMH previous neurology, migraines, epilepsy, eye problems, recent infections, iBP, irregular heart, DM, psychiatric disorder DH focus to sym ptom pattern (eg if peripheral neuropathy, ask about isoniazid, metronidazole) SH alcohol, recreational drugs; FH nerve or muscle problems. Obs BP, HR, GCS (see b p338 if d), glucose . Look for perform a complete neuro exam (b p132) including cerebellar signs; CVS exam for AF and carotid bruit. Investigations these should be determined by the location of the lesion determined by clini cal examination. blds FBC, U+E, Ca2+, glucose, ESR, CRP, autoantibodies; EMG and nerve cond uction studies can help peripheral neuropathy or myopathy; CT/MRI imaging and LP. Urgent CT brainstem or cerebral (lateralising) signs, persistent dGCS, sus- pected subarach noid hemorrhage (b p360), head injury (b p438). Lesion location your aim is to determine which region of the nervous system is aff ected to help target further investigation and aid diagnosis. With motor symptoms there are three m ain areas: \200 Lower motor neuron (LMN) peripheral nervous system; wasting, fasciculatio ns, reduced refl exes and tone, forehead involved if CN VII \200 Upper motor neuron (UMN) central nervous system; increased tone and refl exes with upgoing plantars, if facial weak ness forehead spared \200 Mixed consider motor neuron disease, multiple sclerosis, spinal cord compression (LMN signs at level of compression, UMN signs below), Friedreich \200\231 s ataxia (UMN weakness with absent ankle and knee jerks), syphilis (taboparesis), subacute combined degeneration of the cord. Sensory loss may map to a particular nerve, a nerve root (dermatome), or aff ect one side o f the body up to the level of a signifi cant lesion within the brain or spinal cord (sensor y level). Alternatively, loss may be bilateral and distal ( \200\230glove and stocking \200 \231) suggesting peripheral neuropathy (eg DM). The combination of the anatomical pattern, timecourse and associated features should enable you to make a clinical diagnosis for most lesions. _OHFP.indb 353 _OHFP.indb 353 30/05/2014 16:18 30/05/2014 16:18 O O H H F F P P i i n n d d b b 3 3 5 5 4 4 3 5 4 Table 11.7 Guide to localizing neurological lesions C H A P T E R Motor power Sensory Re \202 exes and tone i1 Features Common causes Stroke (b p351), SOL (b p355), migraine Cerebrum Hemiparesis Hemisensory loss