Creutzfeldt-Jakob disease and prion disease

• Creutzfeldt-Jakob disease (CJD) is a rapidly fatal brain disease caused by a misfolded prion protein that converts the normal protein of nerve cells into more misfolded protein.
• About 85% of cases occur sporadically, usually in older adults; the rest are genetic, acquired after medical procedures, or, in the case of variant CJD, linked to BSE (mad cow disease) exposure.^[5]
• The classic picture is a dementia that worsens week by week, often with myoclonus (sudden brief muscle jerks), ataxia, visual disturbance and akinetic mutism, leading to death in months.
• The diagnosis rests on a typical brain MRI (diffusion restriction, sometimes called cortical ribboning), characteristic EEG changes, cerebrospinal fluid (CSF) biomarkers, and above all RT-QuIC, a highly specific test for misfolded prion protein; genetic testing is offered in young or familial cases.
• There is no disease-modifying treatment; care is supportive and palliative. The most important public health measures concern reusable instruments and donated tissue, because prions resist ordinary sterilisation.

By the end of this page you should be able to:

1. Explain what prions are and how they damage the brain, and name the four main forms of human prion disease.
2. List the clinical red flags of sporadic CJD and interpret the typical MRI, EEG and CSF findings.
3. Apply the international diagnostic criteria for sporadic, inherited and iatrogenic CJD.
4. Explain how sporadic, variant, familial and iatrogenic forms differ in age of onset, presentation, course and brain imaging.
5. State the infection-control precautions that matter for prions and why standard high-level disinfection is not enough.
6. Recognise the common mimics of rapidly progressive dementia and the features that separate them from CJD.
7. Discuss why there is no proven disease-modifying therapy and what the best current evidence supports.

The normal brain prion protein is called PrP^C ("cellular"). It is a cell-surface glycoprotein anchored to neurons by a glycosylphosphatidylinositol anchor. In disease, part of it converts into a misfolded, partially protease-resistant isoform called PrP^Sc (the "scrapie" isoform) that acts as a template: it makes further copies of itself and forms aggregates that disrupt neurons. Prions contain no nucleic acid, so this is a self-propagating protein misfolding disorder rather than a conventional infection. Under particular conditions it is also transmissible.

Human prion disease falls into three broad aetiological groups, several of which are labelled CJD.^[1][2]

• Sporadic CJD (sCJD). The commonest form, roughly 85% of all cases, arising without a known exposure or inherited mutation.^[5] Why the first misfolding event occurs is unknown.
• Inherited (genetic or familial) prion disease. Caused by pathogenic variants in the PRNP gene, which encodes the prion protein. It includes genetic CJD, Gerstmann-Sträussler-Scheinker syndrome (GSS, a slowly progressive syndrome with prominent ataxia) and fatal familial insomnia (FFI, with intractable insomnia, dysautonomia and thalamic degeneration). These forms are clinically variable and often run a longer course than sporadic disease.^[1][2]
• Acquired (iatrogenic) CJD (iCJD). Results from medical exposure to contaminated human tissue or instruments: cadaveric human growth hormone, dura mater grafts, neurosurgical instruments, corneal transplantation and, rarely, blood or blood products. It accounts for less than 1% of human prion disease, but incubation can exceed 30 years.^[1][2]
• Variant CJD (vCJD). The form linked to bovine spongiform encephalopathy (BSE, "mad cow disease") exposure. It has affected young adults, starts with psychiatric or sensory symptoms and takes a longer course, and has been transmitted by blood transfusion from asymptomatic donors.^[1][2]

Human prion disease is rare: the stable worldwide incidence of sporadic CJD is about 1 to 2 cases per million people per year.^[1][2][6] It is nonetheless clinically important because its course is rapid, early recognition is hard, and outcome is invariably fatal.^[1] Sporadic disease becomes more common with age and incidence rises after the sixth decade.^[1] Men and women are affected about equally.

Acquired forms have become exceedingly rare since contaminated growth hormone and dura mater grafts were withdrawn and BSE controls tightened. But the risk has not been eliminated, because incubation can last decades and asymptomatic carriers cannot be reliably identified.^[1] There is also considerable regional and subtype variation: E200K familial disease clusters in parts of Italy, Slovakia and Chile and in some Jewish communities.^[2]

No environmental, dietary, occupational or lifestyle risk factor has been consistently established for sporadic CJD, and it is not contagious through ordinary contact. Exploratory work (for example on gut microbiota) has not produced a modifiable risk factor or a reliable early test.

The PRNP codon 129 polymorphism (methionine versus valine) strongly influences susceptibility and phenotype. Homozygosity for methionine at codon 129 increases susceptibility to sporadic CJD and is present in almost everyone who develops variant CJD.^[1][2]

Different PRNP variants give different syndromes. E200K and similar mutations produce a classical genetic CJD-like illness; V180I tends to run a slower course; D178N coupled with valine at codon 129 gives a CJD phenotype, while D178N coupled with methionine gives fatal familial insomnia.^[1][2] E200K is the commonest mutation worldwide, with clusters in Chile, Italy, Slovakia and Jewish communities in Libya and Tunisia.^[2]

Request PRNP sequencing when there is early onset, an atypical phenotype, or a suggestive family history.^[1]

Iatrogenic risk today is confined to people who have received cadaveric human growth hormone, dura mater or corneal grafts, neurosurgical instruments previously used on an infected patient, or blood and blood products from a future vCJD case. Blood transfusion transmission is documented for vCJD and is linked particularly to products that have not undergone leucodepletion; for sporadic and other forms of CJD routine transfusion transmission has not been established.^[1][2] There is no licensed donor blood screening test.

The basic problem is the same at every scale.^[1][2]

1. Conversion. Cellular PrP^C is refolded into the abnormal isoform PrP^Sc. The two have the same amino-acid sequence but differ in shape and aggregation.
2. Propagation. PrP^Sc is not cleared normally. It seeds conversion of further PrP^C molecules, producing a self-sustaining chain reaction that spreads along neural networks.
3. Damage. The end result is neuronal dysfunction and death, spongiform change in the neuropil, astrogliosis and, in many cases, amyloid plaques. Which brain regions are affected first determines the earliest symptom: memory, cerebellum, vision or behaviour.
4. Transmissibility. Disease spreads when tissue with high infectivity is introduced into a susceptible host. Infectivity is highest in brain, spinal cord and posterior eye; peripheral tissues carry much less, although prion seeding activity has been demonstrated in skin.^[1][5]

A practical consequence: prions resist conventional disinfection and sterilisation. They survive procedures that reliably inactivate bacteria and viruses, so prion infection-control rules differ from ordinary practice.^[1][5]

At post mortem the brain is often small and atrophic. Microscopy shows spongiform change (fine vacuolation of the neuropil), neuronal loss, astrocytic gliosis and deposition of abnormal prion protein. Immunohistochemistry for PrP is diagnostic. Genetic forms can produce more distinctive patterns, such as kuru-type plaques in some MV2 molecular subtypes and the cerebellar amyloid deposition of GSS. A definite diagnosis continues to require neuropathological, immunocytochemical or biochemical confirmation of pathological prion protein.^[1]

The first symptoms are easy to miss because they are non-specific. Recurrent themes in published series are:

• memory loss and confusion
• behavioural change or depression
• unsteadiness and falls
• visual disturbance
• dysphasia or dysarthria

What makes them notable is the tempo: deterioration is measured in weeks rather than years. A person who was independent a month ago is dependent now. That mismatch, a rapid decline in an older adult, is the central red flag.^[2][6]

Psychiatric symptoms deserve special attention. Depression, anxiety, apathy, irritability and behavioural disturbance can dominate the early weeks, especially in older patients and in variant CJD, leading to misdiagnosis as a primary psychiatric illness.^[2][6] Treatment resistance together with early cognitive decline is a warning sign.

As the illness evolves, a multisystem neurological picture appears.^[1][2]

• Cognitive. Rapidly progressive dementia with aphasia, apraxia and executive dysfunction.
• Motor. Myoclonus, often startle-sensitive, is a frequent and supportive sign; pyramidal and extrapyramidal signs, rigidity and tremor may follow.
• Cerebellar. Gait ataxia and limb incoordination; the ataxic molecular subtypes may run slightly longer.
• Visual. Visual field defects, cortical blindness and visual agnosia; in the Heidenhain (visual) variant, visual symptoms lead and dementia follows.
• Bulbar and autonomic. Dysphagia, weight loss, autonomic instability and, ultimately, akinetic mutism.

There is no single sign that proves CJD, but a combination is highly suggestive.^[1][2]

• impaired attention, orientation and memory; sometimes dysphasia.
• myoclonus at rest, on action, or after sudden noise or touch.
• cerebellar ataxia, abnormal extraocular movements.
• hyperreflexia, spasticity or parkinsonism.
• visual field defects or cortical blindness in the visual variant.
• late-stage mutism, rigidity and wasting.

Several pattern-based descriptions help, because the first symptom predicts the dominant deficit.^[1]

• Cognitive pattern - rapidly progressive dementia with executive and language deficits (common in MM1/MV1 and MM2-cortical subtypes).
• Cerebellar pattern - early gait imbalance and ataxia with relatively delayed cognitive decline.
• Visual pattern - visual disturbance progressing to dementia (Heidenhain variant).
• Psychiatric/sensory pattern - prominent early psychiatric symptoms and painful sensory symptoms in vCJD.
• Sleep and autonomic pattern - fatal familial insomnia and related thalamic subtypes: intractable insomnia, dysautonomia, ataxia.

No single sign is pathognomonic; it is rapid progression together with early multisystem involvement that is the valuable clinical signal.

CJD is a cause of rapidly progressive dementia, and the differential is broad. Many mimics are reversible or treatable, so they must be excluded before accepting a prion diagnosis. The table compares the commonest alternatives; particular care is needed with autoimmune encephalitis, because it responds to treatment, and with rapidly progressive Alzheimer or vascular disease.^[1]

A rapidly progressive encephalopathy that worsens week by week should raise prion disease even before the full triad is present.

MRI is the key structural investigation and often becomes abnormal before EEG and CSF biomarkers. Diffusion-weighted imaging provides the highest sensitivity, showing restricted diffusion in the cerebral cortex (the "cortical ribbon") and/or the basal ganglia (caudate and putamen).^[1][6] Involvement of insula, cingulate and frontal cortex with relative sparing of the perirolandic strip is a supportive pattern. FLAIR often shows corresponding hyperintensity. MRI is sensitive and specific enough to miss few cases, but it may be normal early, and serial imaging can be decisive. Preferential thalamic (pulvinar) hyperintensity is a hallmark of variant CJD.^[1][2]

Periodic sharp-wave complexes (PSWC) on a diffusely slowed background occur in roughly two-thirds of sporadic CJD cases, usually in intermediate disease stages.^[1][2][6] They are neither universal nor specific, being uncommon in variant, genetic and many iatrogenic forms, so EEG is a supportive test within an integrated diagnostic framework rather than a primary diagnostic test.^[1]

Lumbar puncture is safe and provides the most informative laboratory support. CSF usually shows a normal cell count and protein.

PRNP sequencing is essential when genetic prion disease is suspected and should be strongly considered in early-onset, atypical or familial cases.^[1] It detects pathogenic variants such as E200K, V180I, D178N and others, and it defines the inherited forms. It also identifies the codon 129 methionine/valine genotype, which has prognostic and epidemiological value.^[1][2]

Computed tomography is rarely abnormal early. Functional (FDG-PET or SPECT) imaging may show cortical and subcortical hypometabolism or hypoperfusion in atypical cases with inconclusive MRI, but it is less specific than MRI diffusion-weighted imaging and RT-QuIC.^[1]

EEG, MRI, CSF biomarkers, PRNP sequencing and neuropathology together form the full diagnostic battery. PET and CT only support.

The international criteria used in surveillance and clinical practice come from the World Health Organization and the International Creutzfeldt-Jakob Disease Surveillance Network. They classify a case as definite, probable or possible, and they partly overlap between forms.^[1]

• Definite sCJD. A progressive neuropsychiatric syndrome with neuropathological, immunocytochemical or biochemical confirmation of pathological prion protein.
• Probable sCJD. One of the following:
  • rapidly progressive cognitive impairment plus at least two of these features: myoclonus, visual or cerebellar disturbance, pyramidal or extrapyramidal signs, akinetic mutism; and either a typical EEG (periodic sharp-wave complexes) or a typical MRI pattern.
  • rapidly progressive cognitive impairment plus at least two of the above clinical features and a positive CSF 14-3-3 protein.
  • a progressive neuropsychiatric syndrome with a positive CSF RT-QuIC result, after exclusion of alternative diagnoses.
• Possible sCJD. Rapidly progressive cognitive impairment plus at least two of the above clinical features, disease duration under 2 years, without a supportive test.^[1]

Most clinicians now regard a positive RT-QuIC in the correct clinical and imaging context as sufficient for a probable diagnosis, and neuropathology is only available when biopsy or post-mortem is possible.

Diagnosis differs from sporadic CJD mainly by the presence of a clearly identifiable iatrogenic exposure; clinical features and laboratory findings largely overlap.^[1]

• Definite iCJD. Mandatory neuropathological confirmation (autopsy or brain biopsy showing pathological prion protein).
• Probable iCJD. A rapidly progressive neurological syndrome compatible with CJD (dementia, ataxia, myoclonus, pyramidal or extrapyramidal signs); supportive CSF and instrumental findings (positive 14-3-3, RT-QuIC, characteristic MRI hyperintensity, EEG periodic sharp-wave complexes); plus a documented history of iatrogenic exposure.

There are no criteria uniquely specific to iCJD; the documented exposure is the distinguishing element.^[1]

Diagnosis requires a progressive neurological syndrome compatible with CJD (rapidly progressive dementia, myoclonus, ataxia, pyramidal or extrapyramidal signs, or visual and psychiatric disturbances) together with a positive family history or an identified pathogenic PRNP mutation.^[1]

• Definite familial CJD. Neuropathological confirmation, or genetic confirmation of a known pathogenic PRNP mutation.
• Probable familial CJD. A compatible syndrome plus a family history and supportive CSF biomarkers and/or characteristic MRI, without genetic or neuropathological confirmation.
• Possible familial CJD. A compatible syndrome and family history, without typical biomarker or imaging findings.

More than 20 pathogenic PRNP mutations are recognised, often with marked clinical heterogeneity, so genetic sequencing is required rather than a clinical guess.^[1]

Consensus vCJD criteria exist in the surveillance literature (young onset, early psychiatric prodrome, painful sensory symptoms, ataxia, dementia, delayed myoclonus, the pulvinar sign on MRI), but because our sources do not reproduce them in full, they are summarised here at teaching level only. Suspect vCJD in a young person with new psychiatric symptoms, painful paraesthesiae, ataxia and a pulvinar sign on MRI, and confirm with the national referral centre's testing pathway.

There is no licensed or proven disease-modifying therapy for any human prion disease; treatment is symptomatic and supportive.^[1][4] Decline is rapid, median survival is typically less than one year from symptom onset overall^[4], and about 4-6 months in sporadic cases^[1], so the window in which an experimental agent might work is small.

A large number of repurposed and mechanism-based agents have been tested. Quinacrine 300 mg/day by mouth produced no difference in survival or function in late-stage CJD; doxycycline 100 mg/day by mouth likewise failed.^[4][7] Monoclonal antibodies against the prion protein (PRN100, administered intravenously to six patients with CJD under a Special License framework) reached pharmacologically relevant concentrations in CSF and was broadly tolerated, but no efficacy on function or survival was shown.^[4] Other approaches (antisense oligonucleotides, small interfering RNA, modulation of brain cholesterol metabolism such as efavirenz) are in early development and have not yet demonstrated clinical benefit.^[4]

This is the real management, and it dominates day to day.^[4]

• Communication early. Discuss prognosis and advance care planning before severe cognitive or speech decline removes the patient's voice; the illness progresses over weeks.
• Symptoms. Treat myoclonus and seizures with anticonvulsants, painful spasms and anxiety with appropriate analgesia or anxiolytics, sleep disturbance and agitation with environmental measures and short-term medication, and dysphagia with texture modification, thickened fluids and, if consistent with the patient's wishes, tube or percutaneous feeding.
• Nutrition and fluids. Avoid unnecessary interventions if they do not match the patient's goals; enteral access is justified only when swallowing fails and the patient has consented.
• Nursing. Pressure-area care, infection-avoidance, aspiration precautions, constipation, and family support.
• Family support. In inherited disease, genetic counselling and, when a mutation is found, cascade testing of relatives.
• Pain and distress. A low threshold for palliative input; the terminal phase is short but can be difficult.

Routine patient contact is safe: CJD is not transmitted person to person through standard care, so isolation and transmission-based precautions are not routinely indicated.^[5] The risk is iatrogenic, via contaminated instruments or donor tissue. Prions resist conventional cleaning, so high-risk reusable instruments (those contacting brain, spinal cord or posterior eye) must never be reprocessed for reuse by the ordinary high-level disinfection route.^[1][5]

Practical principles, which align with CDC, WHO and national guidance:^[1]

• Use single-use instruments where possible for any procedure on a suspected or confirmed case; discard after use. If reusable surgical instruments must be used, treat them as heavily contaminated, clean, sterilise by validated prion methods, and then incinerate rather than return to service.^[1][5]
• CDC 2026 guidance on surgical instrumentation recommends soaking in a 2-molar (2 M) sodium hydroxide solution or undiluted sodium hypochlorite for 1 hour.^[5] WHO (1999 infection-control guidelines for transmissible spongiform encephalopathies) recommends that heat-sensitive instruments exposed to CJD be immersed in sodium hypochlorite for 1 hour before reprocessing.^[5]
• Peracetic acid is considered ineffective for prion inactivation under the conditions of standard high-level disinfection at room temperature, so peracetic-acid-based reprocessing is not relied upon for prion decontamination.^[5]
• Instruments that have contacted high-infectivity tissue should not be reused unless validated prion decontamination has been carried out.^[1]
• CSF and tissue samples are collected and transported with standard precautions (gloves, eye protection), double-bagged, labelled "possible CJD", and hand-delivered. Laboratories then follow enhanced precautions: disposable gowns, face protection and processing in a biological safety cabinet, with bleach-based surface disinfection and incineration of waste.^[5]
• National bodies including UKHSA, the CDC and WHO publish prion infection-control guidance; they agree on these central principles even where details, such as endoscope handling, differ between countries.

Surgery should be avoided unless essential. If a procedure cannot be deferred, involve infection control early, review the reusable instrument plan, and prefer interventional-radiology or percutaneous approaches using single-use kit. Gastric and other non-central-nervous-system tissues are not considered high infectivity, but the absence of documented transmission is not the same as absence of risk.

• Aspiration pneumonia and malnutrition from dysphagia.
• Falls, fractures and infection from immobility.
• Seizures and myoclonic jerks that disrupt sleep and care.
• Complications of gastric or enteral feeding (aspiration, displacement) if used.
• Family distress, bereavement and, in inherited disease, the psychological impact of a heritable fatal diagnosis.
• Care burden: rapid decline in weeks to months after a long diagnostic delay.

Prognosis is poor in every form. In sCJD, survival is typically measured in months: a mean of about four months in some series, with most patients dying within 4-6 months, up to 6-12 months at the extremes.^[1][2] Variant CJD usually runs longer, 12-24 months, but still ends in death.^[1] Iatrogenic and genetic forms vary; some, such as GSS and FFI, may progress over years. There is no recovery, no arrest, and no meaningful response to symptomatic therapy so far.^[1][4] Early recognition matters mainly for patient safety (procedures), family counselling and the exclusion of treatable mimics.

• There is no vaccine and no proven preventive drug for prion disease.
• Donor tissue and blood. Exclusion of donors with suspected prion disease, and use of leucodepleted blood products, reduce iatrogenic risk.^[1][2]
• Instruments and environment. Single-use or incineration policies prevent cross-transmission.^[1][5]
• Neurosurgical traceability. Instruments used on a case are tracked, quarantined or destroyed; the relevant notification (such as "rule-out CJD") is placed in the record before surgery is scheduled.
• Screening of tissue. Some countries (for example, the Czech Republic since 2007) perform mandatory Western blot testing of corneal donor brain tissue, an approach that could be extended using more sensitive prion amplification assays such as RT-QuIC or PMCA in high-risk tissues.^[1][8]
• Surveillance. National and international surveillance networks (for example, through the WHO and International Surveillance Network) exist to monitor incidence and to catch atypical cases early.^[1]

Carriers and first-degree relatives of a patient with familial prion disease need genetic counselling before testing, and a clear plan for disclosing results. Where a pathogenic PRNP variant is identified, at-risk relatives may be offered predictive testing with support, and (in research) enrolment in early-intervention or surveillance studies. PRNP codon 129 data add prognostic and epidemiological context.^[1][2]

Myoclonus in a teenager is commoner for other reasons. When a young person has a rapidly progressive encephalopathy, prion disease is rare but must be considered; think especially of vCJD in the young (median age at death about 28, psychiatric prodrome, longer course) and of inherited disease. Variant CJD has been documented in children in the UK under active surveillance.^[1][2]

no source gives pregnancy-specific management or evidence for CJD. Principles are the same as in other adults (supportive care, infection control, genetic counselling) and management should be shared between neurology and obstetrics. Most vCJD and iCJD acquired in the past means presentation in young adults is rare now.

Missed diagnosis is most common here: new depression, weight loss and cognitive decline attributed to ageing, depression or a primary psychiatric illness. Late-onset psychiatric symptoms with rapid cognitive decline in an older adult should lower the threshold for diffusion-weighted MRI.^[6]

Recipients of older corneal or dura grafts, or of cadaveric growth hormone before purification changes, remain at (very small) risk of iatrogenic CJD decades later. Ask about such history in any young-onset rapidly progressive dementia.

• The diagnosis can be strongly suspected without advanced tests: a dementia that worsens week by week, myoclonus developing after cognitive decline, ataxia and visual disturbance. In adolescents or young adults, think variant CJD.
• MRI with diffusion-weighted imaging is the single best test; if unavailable, EEG and clinical judgement are the main supports, with CSF 14-3-3 where the assay exists.
• RT-QuIC is not available in many settings; a negative result would not be expected to change management in a clinically obvious case, but a positive result confirms it. Even without RT-QuIC, the WHO 1998 criteria (clinical picture plus 14-3-3 or MRI/EEG) allow a probable diagnosis.^[3]
• Infection control depends on habits rather than technology: single-use instruments, destruction (burning) of contaminated items, and avoiding reuse of reusable surgical instruments used on brain or spinal cord.
• Care is supportive. Identify palliative services early; family should be told the prognosis is poor but not that all hope for comfort is lost.

• CJD is a rapidly fatal prion disease: abnormal PrP^Sc templated conversion of normal PrP^C, producing spongiform change and neuronal death.
• About 85% of cases are sporadic with incidence 1-2 per million per year and typical age 50-75 years; other forms are genetic, iatrogenic and (BSE-related) variant.^[5][1]
• The presentation is a dementia measured in weeks, plus myoclonus, ataxia, visual disturbance and psychiatric change; the tempo is the red flag.
• MRI diffusion-weighted imaging (cortical ribboning and/or basal ganglia restriction) and EEG periodic sharp-wave complexes are the main imaging and electrophysiological clues.
• CSF RT-QuIC has around 99% specificity and over 90% sensitivity in second-generation assays; it is the most informative CSF test. 14-3-3 (70-85% sensitivity in one review, 85-92% in another) and total tau support but are not specific.^[1][6][3]
• Diagnostic criteria (WHO/International Surveillance Network) classify cases as definite (neuropathology), probable (clinical plus supportive test) or possible; genetic and iatrogenic forms have additional requirements (PRNP mutation, documented exposure).
• Variant CJD affects young adults, begins with psychiatric or sensory symptoms, shows the pulvinar sign, and can be blood-borne.
• Iatrogenic CJD can emerge decades after exposure (growth hormone, dura mater, corneal grafts, neurosurgical instruments).
• Genetic forms require PRNP sequencing; codon 129 methionine homozygosity increases susceptibility and is present in almost all vCJD.
• No proven disease-modifying treatment exists: quinacrine 300 mg/day, doxycycline 100 mg/day and PRN100 have all failed to show efficacy.^[4][7]
• Care is supportive and palliative, with particular attention to advance care planning, myoclonus, dysphagia and family support.
• Prions resist standard sterilisation: use single-use instruments, avoid high-level disinfection (peracetic acid is ineffective at room temperature) and incinerate contaminated reusable instruments.
• Standard precautions are enough for routine bedside care; isolation is not routinely required.
• Prognosis is months: about 4-6 months in sporadic disease, 12-24 months in variant disease.^[1]
• Prevention rests on donor screening and tissue handling, surveillance, blood leucodepletion and strict instrument control rather than on drugs or vaccines.

Plain-text links to nearby MedGrasp topics (listed while awaiting verification status): Lewy body dementia; rapidly progressive dementia; autoimmune encephalitis; dementia with Lewy bodies; Alzheimer disease; EEG interpretation; infection control and sterilisation in practice.