Home > News > How Reversible are ‘Reversible Dementias’?
Alzheimer's Disease & Dementia
Read Time: 8 mins

How Reversible are ‘Reversible Dementias’?

Published Online: January 3rd 2012 European Neurological Review, 2011;6(4):230-233 DOI: http://doi.org/10.17925/ENR.2011.06.04.230
Authors: Panagiotis Ioannidis, Dimitris Karacostas
Quick Links:
Abstract
Article
Article Information
Abstract:
Overview

Reversible dementias comprise different groups of disorders of variable aetiologies, such as structural brain lesions or metabolic, infectious, toxic, autoimmune, paraneoplastic and psychiatric disorders. When patients present with cognitive symptoms, especially in the younger age groups, the first thought of the attending neurologist should be to try to identify an underlying treatable cause. The incidence of degenerative dementia rises with older age and its symptoms progressively become more evident and typical; in such cases, a differential diagnosis is limited and the chance of uncovering a treatable disorder is minimal. However, although uncommon, treatable dementias or dementia-like symptoms do exist. Future studies with better design and methodology, as well as longer observation periods and larger patient populations, are needed to clarify the controversial issues concerning the epidemiology and accurate diagnosis of, and treatment possibilities for, reversible dementias.

Keywords

Reversible dementia, classification, differential diagnosis, treatment, review

Article:

Dementia is a syndrome that can have multiple causes and is characterised by deterioration in different domains of cognition, especially memory, language, praxis, visual perception and executive function.1 It is estimated that the number of people with dementia will increase dramatically over the next few decades,2 presenting a tremendous burden for patients, spouses and other family carers, and society. Consideration of the differential diagnosis of dementia is a complex process, and accurate diagnosis is challenging. Primary degenerative dementias result from irreversible aetiologies, such as beta-amyloid deposition, inclusion of Lewy bodies, taupathies or other dysfunctional proteins, whereas reversible dementias are secondary to other treatable conditions. When patients present with cognitive symptoms, especially in the younger age groups, the first thought of the attending neurologist should be to try to to identify an underlying treatable cause. Reversible dementias comprise different groups of variable aetiologies, such as structural brain lesions or metabolic, infectious, toxic, autoimmune, paraneoplastic and psychiatric disorders.3 The aim of this article is first to define these treatable conditions and second to explore how reversible they really are according to data from the literature.4,5

Traditional and New Approach to Reversibility

Between the 1980s and early 1990s, most studies estimated the prevalence of reversible dementias to be almost 20 %, introducing aetiologies such as normal pressure hydrocephalus (NPH), structural brain abnormalities, depression, hypothyroidism and vitamin B12 deficiency.6,7 However, many of these studies were lacking strict criteria, adequate follow-up and solid methodology.8
In recent years, neurologists have taken a new approach to reversibility. It seems that good history evaluation, clinical examination accompanied by certain psychometric tests and appropriate laboratory work-up should be considered for every patient with cognitive symptoms.9 The incidence of degenerative dementia rises with older age and its symptoms progressively become more evident and typical; in such cases, the differential diagnosis is limited and the chance of uncovering a treatable disorder is minimal.10 However, in patients with younger onset dementia, the process is different. The possibility of revealing a reversible cause is higher and the differential diagnosis and work-up are broadened.11
Different possible causes of reversible dementias or dementia-like symptoms are summarised in Table 1 and detailed below.

Traditional Causes of Reversible Dementias
Structural Brain Lesions

NPH presents with the classical triad of gait disturbance, memory complaints and urinary incontinence. However, not all patients with NPH show improvement after cerebrospinal fluid drainage. Depending on the time of shunting, urinary incontinence and gait apraxia may resolve and memory may improve.12 In the long term, full reversibility is unlikely if there is a parallel degenerative illness or a concomitant true dementia.13
Patients with subdural haematomas and brain tumours are likely to see a resolution of their cognitive symptoms after surgical treatment.

Alcoholic Dementia

Deterioration in cognition, behavioural changes and personality changes are well known to result from chronic alcohol abuse. The role of alcohol in the dementia process is still debated. It is not clear whether there is a direct toxic effect or a secondary cognitive decline due to other factors related to alcohol consumption. Abstinence may improve cognition, but true reversibility is uncertain.14

Nutritional Disorders

The role of vitamin B12 deficiency in neurological disorders has been known for many years. Vitamin B12 deficiency may cause subacute combined degeneration, psychiatric symptoms, multiple-sclerosis-like syndrome, delirium and dementia or cognitive impairment.15 It was thought that, after B12 supplementation in patients with low serum cobalamin, dementia would resolve. However, most studies lack evidence of this.16,17 Vitamin B12 deficiency may be an epiphenomenon of dementia rather than a cause of cognitive deterioration.18
Wernicke’s encephalopathy and Korsakoff’s syndrome are potentially treatable after alcohol withdrawal and nutritional supplementation. Wernicke’s encephalopathy is characterised by the triad of opthalmoparesis, ataxia and confusion, and is a consequence of thiamine deficiency. Brain magnetic resonance imaging (MRI) shows atrophy of mammillary bodies and insult of the median thalamus.19

Endocrine Disorders

Thyroid disturbances, such as hypothyroidism and hyperthyroidism, can potentially cause depression and memory dysfunction. With the stabilisation of thyroid function, mood and memory may return to normal.20 However, many people with dementia present with abnormal thyroid tests in their blood tests or history.
Idiopathic hypoparathyroidism is a rare disorder that causes cerebral calcification or Fahr’s disease. As the disease progresses, dementia appears, together with other neurological complications such as epilepsy, Parkinsonism and raised intracranial pressure. Treatment is mainly symptomatic and dementia symptoms partially resolve.21

Metabolic Disorders

Electrolyte disturbances and hepatic, renal or pulmonary insufficiency may present as transient cognitive impairment that can mimic dementia. Cognition may be restored after treatment of the underlying disorder.
Wilson’s disease is an autosomal recessive disorder of copper metabolism. Manifestations include psychiatric and movement abnormalities resulting from copper accumulation and toxicity. Treatment is through chelation with trientine and zinc supplementation. Cognitive symptoms are also present and improve with therapy.22

Toxic Conditions

Exposure to toxic agents may occur in some professions and cause neurocognitive impairment. For example, lead exposure causes lead encephalopathy in industrial workers. Heavy metals such as mercury, bismuth, aluminium, manganese and arsenic have also been implicated in dementia symptoms. Carbon monoxide intoxication can present with confusion and altered memory. Most of these symptoms are often not reversible; however, sequestration of the offending agent may prevent further clinical decline.23

Psychiatric Disorders

Depression in older people was initially thought to cause dementia-like symptoms. However, depression may actually be the first symptom of a dementia illness.24 Older people who were treated for depression showed improvement in cognition without absolute reversibility of dementia, indicating a possible overlap between the two conditions in older patients.25 However, the question still is: does pseudodementia really exist or are we dealing with pseudo pseudodementia?

Miscellaneous Causes

Many other heterogeneous conditions have been shown to be involved in the reversible dementia pathogenesis. For example, dementia cases due to radiation or dialysis have been reported to reverse after appropriate treatment.26 The identification of such conditions is easier when patients’ previous history is considered.

New Causes of Reversible Dementias
Epileptic Disorders

Transient epileptic amnesia is a syndrome characterised by recurrent, brief attacks of memory loss in middle-aged or older people, usually after sleep, associated with symptoms of temporal lobe epilepsy (automatisms, electroencephalogram findings, etc.). It is a benign syndrome that is responsive to antiepileptic medication, but complete resolution of cognitive symptoms is unusual.27 It has been suggested that a degenerative process exists in parallel with the epileptic disorder.28

Autoimmune Encephalopathies

Autoimmune encephalopathies (or autoimmune dementias) is a newly proposed term for dementias underlying an autoimmune process. They constitute a heterogeneous group of disorders that may present with cognitive decline.29 With the discovery of antibodies such as anti-Yo, anti-Hu and anti-Ri, which are related to paraneoplastic disorders, the spectrum of potentially treatable dementias has been broadened. Also, a specific search for other antibodies – such as voltage-gated potassium channel antibodies in non-paraneoplastic encephalopathies and anti-N-methyl-d-aspartate receptor antibodies in paraneoplastic encephalopathies30,31 – has demonstrated that reversible dementias are not a myth. A favourable prognosis is achieved with resection of the underlying tumour and/or immunosuppression in paraneoplastic cases, and with appropriate management using immunosuppression in non-paraneoplastic cases.
Hashimoto’s encephalopathy is another potentially treatable disorder that presents as rapidly progressive dementia accompanied by myoclonus, epileptic seizures and altered level of consciousness. Brain computed tomography or MRI may be normal but thyroid antibodies (anti-thyroid peroxidase and anti-thyroglobulin) can be found in high titres. Steroid initiation is the treatment of choice, with immediate improvement (steroid-responsive encephalopathy).32

Obstructive Sleep Apnoea

Some patients referred to memory clinics are suffering from obstructive sleep apnoea. These patients are often younger and may represent around 5 % of patients under 65 years attending these clinics.33 Due to the bad quality of sleep and the excessive daytime sleepiness, memory problems may be the first symptoms these patients experience. Improvement in memory is evident after treatment.

Inflammatory Vasculopathies

Other inflammatory or autoimmune diseases may present with central nervous system (CNS) involvement. Systemic lupus erythematosus, Sjögren’s syndrome, Behçet’s disease, antiphospholipid syndrome and sarcoidosis can affect CNS vasculature.34 Isolated CNS angiitis is another condition that may initially present with cognitive symptoms.35 The diagnosis of these disorders is usually difficult and requires a high degree of suspicion.
Primary CNS angiitis is a rare autoimmune disease that typically presents in middle-aged people with headache, cognitive symptoms, stroke and seizures. Angiitis of the CNS may have a fluctuating course or a stepwise rapid deterioration that could be misleading. The diagnosis is confirmed by conventional angiography or brain biopsy and the recommended treatment is a combination of corticosteroids and immunosuppression. Relapses are not unusual.
CNS sarcoidosis may also present with dementia symptoms. It is a multisystem granulomatous disease that commonly affects the lungs, eyes and skin. The condition is difficult to diagnose but is responsive to steroids. With early treatment, reversal of symptoms may occur.36

Vascular Causative Factors

Dural arteriovenous fistulae (DAVF) have been associated with progressive cognitive dysfunction. These lesions often occur with focal neurological symptoms or signs, but cognitive impairment may be the sole manifestation.37 The prognosis after selective embolisation is very good, with complete resolution of the symptoms. Magnetic resonance angiography and catheter angiography show venous flow reversal and decreased perfusion of the cerebral parenchyma. Diagnosis is difficult, but DAVF should be in the differential diagnosis of atypical cases with subacute cognitive decline. It is hypothesised that the symptoms and imaging findings result from venous hypertension.

Infections

Infections of the CNS such as cryptococcal meningitis, Lyme disease, Whipple’s disease, syphilis and HIV could induce dementia symptoms. Early management of these infections may result in reversibility of the cognitive impairment. However, permanent damage and irreversibility of the cognitive symptoms is not an unusual scenario in untreated or undetected cases.
Whipple’s disease is very rare. The incidence is about 5–10 cases in one million every year. It can affect the CNS and present as dementia without gut involvement. It is difficult to diagnose, but treatable if managed when symptoms first start.38 Lyme disease is another treatable infection that can affect the CNS and present as dementia.39
Cognitive symptoms are a late complication of neurosyphilis. Diagnosis is easy and based on the evaluation of serology for Treponema pallidum. Syphilis is a common complication in immunocompromised patients.40 Serological tests for Treponema should be available in everyday clinical practice, as the incidence of the disease has risen in recent years due to people migrating from underdeveloped countries.
HIV dementia is irreversible, but HIV-related neurocognitive impairment may be reversed by highly active antiretroviral therapy. Treatment response is strongly related to the neurocognitive status of the patient prior to initiation of treatment.41

Medications

There are several reports of drugs that have provoked cognitive impairment, especially in older people who are susceptible to polypharmacy and drug–drug interactions.42,43 Benzodiazepines, antipsychotics, antiepileptics and tricyclic antidepressants have been accused of worsening memory and executive functioning. Newer and older antiepileptic drugs, such as topiramate and sodium valproate, have been implicated in worsening cognition.44,45 Cognitive symptoms may be reversed after withdrawal of the responsible drug. Steroid psychosis is a well known adverse event of chronic steroid treatment. In contrast, steroid dementia is still debated. There are well documented reports showing that cognitive problems have resolved after steroid discontinuation.46 In experimental rat models, the use of corticosteroids affects the hippocampus and induces dysfunction in cognition.47

Discussion

As we have shown, reversible dementias comprise a group of diseases with different aetiologies. With a detailed history, a thorough clinical examination and sometimes extensive laboratory investigations, a treatable cause of dementia is often difficult to be reached but can alter the patient’s progress. Traditional treatable dementias, such as those arising from NPH, brain tumours, B12 deficiency, endocrine disorders and depression, are partially reversible.48 Reversibility depends on the time of diagnosis and concomitant medical problems. In vitamin B12 deficiency, for example, if supplementation can be started early, stabilisation of memory complaints and improvement may be seen – however, many people with dementia present with low serum B12 concentrations.49 The same may happen with NPH after shunting. Some of the symptoms may improve and stabilise, but the condition is not fully reversed.
For autoimmune dementias, with an accurate diagnosis and early treatment, the chance of reversibility is higher.50 However, other issues arise in these patients. How long should they receive treatment, and which medication would be the safest to use? In Hashimoto’s encephalopathy, the condition may relapse after steroid tapering or discontinuation.51
In dementias with an infectious cause, such as HIV, early drug intervention is crucial as they are reversible, at least in the first stages.
In younger patients with atypical presentation or a rapidly progressive disease course, a brain biopsy, although invasive, should be the final investigation to rule out or confirm an inflammatory or autoimmune process,52 especially if other investigations have failed to reveal a cause. However, in a number of such patients, a biopsy may only show non-specific findings and it will not be possible to reach a firm conclusion, even after such an invasive procedure.
In recent years, as neurologists have approached reversibility from a different angle, the prevalence of reversible dementias has decreased.53 The traditionally quoted figure of a 20 % prevalence has been mostly abandoned.54 A new look at an old problem shows that true reversibility is rare (1 %)55 and uncommon in older patients with cognitive decline who fulfil the proposed criteria for primary degenerative dementia. In contrast, in younger patients, especially those experiencing a rapid deterioration of their cognitive abilities, further diagnostic work-up with newly recognised antibodies and specific serological tests is highly warranted.
In conclusion, although uncommon, treatable dementias or dementia-like symptoms do exist,56 but their actual prevalence is not known. Future studies with better design and methodology, as well as longer observation periods and larger patient populations, are needed to clarify the controversial issues concerning the epidemiology and accurate diagnostic of, and treatment possibilities for, reversible dementias. ■

Article Information:
Disclosure

The authors have no conflicts of interest to declare.

Correspondence

Panagiotis Ioannidis, AHEPA University Hospital, St Kyriakidi 1, 54636, Thessaloniki, Greece. E: ioannidispanosgr@yahoo.gr

Received

2011-07-14T00:00:00

References

  1. Knopman DS, DeKosky ST, Cummings JL, et al., Practice parameter: diagnosis of dementia, Neurology, 2001;56:1143–53.
  2. Ferri CP, Prince M, Brayne C, et al., Alzheimer’s Disease International. Global prevalence of dementia: a Delphi consensus study, Lancet, 2005;366:2112–7.
  3. Kabasakalian A, Finney GR, Reversible dementias, Int Rev Neurobiol, 2009;84:283–302.
  4. Piccini C, Bracco L, Amaducci L, Treatable and reversible dementias: an update, J of Neurol Scien,1998;153:172–81.
  5. Weytingh M, Bossuyt P, van Crevel H, Reversible dementia: more than 10% or less than 1%? A quantitative review, J Neurol, 1995;242:466–71.
  6. National Institute on Aging Task Force, Senility reconsidered: treatment possibilities for mental impairment in the elderly, JAMA, 1980;244:259–63.
  7. Rabins PV, The reversible dementias. In: Arie T (ed.), Recent Advances in Psychogeriatrics, Edinburgh, Scotland: Churchill Livingstone, 1985:93–102.
  8. Barry P.P, Moskowitz M.A, The diagnosis of reversible dementia in the elderly: A critical review, Arch Intern Med, 1988;148:1914–8.
  9. Knopman DS, Boeve BF, Petersen RC, Essentials of the proper diagnoses of mild cognitive impairment, dementia, and major subtypes of dementia, Mayo Clin Proc, 2003;78:1290–308.
  10. Lobo A, Launer LJ, Fratiglioni L, et al, Prevalence of dementia and major subtypes in Europe: A collaborative study of population-based cohorts. Neurologic Diseases in the Elderly Research Group, Neurology, 2000;54(11 suppl. 5):S4–9.
  11. Rossor M, Fox N, Mummery C, The diagnosis of young onset dementia, Lancet, 2010;9:793–806.
  12. Aygok G, Marmarou A, Young HF, Three year outcome of shunted idiopathic NPH patients, Acta Neurochir Suppl, 2005;95:241–5.
  13. Hamilton R, Patel S, Lee EB, et al., Lack of shunt response in suspected idiopathic normal pressure hydrocephalus with Alzheimer disease pathology, Ann Neurol, 2010;68(4):535–40.
  14. Victor M, Alcoholic dementia, Can J Neurol Sci, 1994;21(2):88–99.
  15. Kalita J, Misra UK, Vitamin B12 deficiency neurological syndromes: correlation of clinical, MRI and cognitive evoked potential, J Neurol, 2008;255(3):353–9.
  16. Teunisse S, Bollen AE, van Gool WA, et al., Dementia and subnormal levels of vitamin B12: effects of replacement therapy on dementia, J Neurol, 1996;243(7):522–9.
  17. Cunha UG, Rocha FL, Peixoto JM, et al., Vitamin B12 deficiency and dementia, Int Psychogeriatr, 1995;7:85–8.
  18. Loikas S, Koskinen P, Irjala K, et al., Vitamin B12 deficiency in the aged: A population-based study, Age Ageing, 2007;36:177–83.
  19. Zuccoli G, Santa Cruz D, Bertolini M, et al., MR imaging findings in 56 patients with Wernicke encephalopathy: nonalcoholics may differ from alcoholics, Am J Neuroradiol, 2009;30(1):171–6.
  20. Dugbartey AT, Neurocognitive effects of hypothyroidism, Arch Int Med, 1998;13:1413–8.
  21. Stuerenburg H J, Hansen HC, Thie A, et al., Reversible dementia in idiopathic hypoparathyroidism associated with normocalcemia, Neurology, 1996;47:474–6.
  22. Flicker L, Ames D, Metabolic and endocrinologic causes of dementia, Int Psychogeriatr, 2005;17:S79–S92.
  23. Schofield P, Dementia associated with toxic causes and autoimmune diseases, Int Psychogeriatr, 2005;17(Suppl.):S129–S47.
  24. Berger AK, Fratiglioni L, Forsell Y, et al., The occurrence of depressive symptoms in the preclinical phase of AD: a population-based study, Neurology, 1999;53:1998–2002.
  25. Wright AL, Persad C, Distinguishing between depression and dementia in older persons: Neuropsychological and neuropathological correlates, J Geriatr Psychiat Neurol, 2007;20:189–98.
  26. Rob PM, Niederstadt C, Reusche E, Dementia in patients undergoing long-term dialysis: aetiology, differential diagnoses, epidemiology and management, CNS Drugs, 2001;15(9):691–9.
  27. Ioannidis P, Balamoutsos G, Karabela O, et al, Transient epileptic amnesia in a memory clinic setting: a report of 3 cases, Epilepsy Behav, 2011;20(2):414–7.
  28. Butler CR, Graham KS, Hodges JR, et al., The syndrome of transient epileptic amnesia, Ann Neurol, 2007;61:587.
  29. Vernino S, Geschwind M, Boeve B, Autoimmune encephalopathies, Neurologist, 2007;13:140– 7.
  30. Schott, MJ, Limbic encephalitis: a clinician’s guide, Practical Neurol, 2006;6:143–53.
  31. Dalmau J, Gleichman AJ, Hughes EJ, et al., Anti-NMDAreceptor encephalitis: case series and analysis of the effects of antibodies, Lancet Neurol, 2008;7(12):1091–8.
  32. Mocellin R, Walterfang M, Velakoulis D, Hashimoto's encephalopathy : epidemiology, pathogenesis and management, CNS Drugs, 2007;21(10):799–811.
  33. Panegyres PK, Frencham K, Course and causes of suspected dementia in young adults: a longitudinal study, Am J Alzheimers Dis Other Demen, 2007;22:48–56.
  34. Rosenbloom MH, Smith S, Akdal G, et al., Immunologically Mediated Dementias, Curr Neurol Neurosci Rep, 2009;9(5):359–67.
  35. Birnbaum J, Hellmann DB, Primary angiitis of the central nervous system, Arch Neurol, 2009;66(6):704–9.
  36. Hoitsma E, Faber CG, Drent M, et al., Neurosarcoidosis: a clinical dilemma, Lancet Neurol, 2004;3:397–407.
  37. Wilson M, Doran M, Enevoldson TP, Cognitive profiles associated with intracranial dural arteriovenous fistula, Age Ageing, 2010;39(3):389–92.
  38. Rossi T, Haghighipour R, Haghighi M, et al., Cerebral Whipple’s disease as a cause of reversible dementia, Clin Neurol Neurosur, 2004;107:258–61.
  39. Wokke J, Vanneste J, Neuroborreliosis, Practical Neurology, 2004;4:152–61.
  40. O’donnel l JA, Emery CL, Neurosyphilis: a current review, Curr Infect Dis Rep, 2005;7(4):277–84.
  41. Tozzi V, Balestra P, Bellagamba R, et al., Persistence of neuropsychological deficts despite long-term highly active antiretroviral therapy in patients with HIV-related neurocognitive impairment, J Acq Immun Def Synd, 2007;45:174–82.
  42. Moore AR, O’Keefe ST, Drug-induced cognitive impairment in the elderly, Drugs Ageing, 1999;15(1):15–28.
  43. Hajjar ER, Hanlon JT, Artz MB, et al., Adverse drug reaction risk factors in older outpatients, Am J Geriatr Pharmacother, 2003;1(2):82–9.
  44. Sempere AP, Medrano V, Berenguer-Ruiz L, Reversible dementia secondary to topiramate, Clin Neuropharmacol, 2008;31(1):62
  45. Beyenburg S, Back C, Diederich N, et al., Is valproate encephalopathy under-recognized in older people? A case series, Age and Ageing, 2007;36:344–6.
  46. Wolkowitz OM, Lupien SJ, Bigler E, et al., The "steroid dementia syndrome": an unrecognized complication of glucocorticoid treatment, Ann N Y Acad Sci, 2004;1032:191–4
  47. Sapolsky RM, Glucocorticoids, Stress and exacerbation of excitotoxic neuron death, Semin Neurosci, 1994;6:323–31.
  48. Alexopoulos GS, Meyers BF, Young RC, et al., The course of geriatric depression with “reversible dementia”: a controlled study, Am J Psychiatry, 1993;150:1693–9.
  49. Clark R, Smith AD, Jobst KA, et al., Folate, vitamin B12 and serum homocysteine levels in confirmed Alzheimer disease, Arch Neurol, 1998;55:1449–55.
  50. Flanagan EP, McKeon A, Lennon VA, et al., Autoimmune dementia: Clinical course and predictors of immunotherapy response, Mayo Clin Proc, 2010;85(10):881–97.
  51. Marshall GA, Doyle JJ, Long-term treatment of Hashimoto’s encephalopathy, J Neuropsychiatry Clin Neurosci, 2006;18(1):14–20.
  52. Warren JD, Schott MJ, Fox CN, et al., Brain biopsy in dementia, Brain, 2005;128(9):2016–25.
  53. Clarfield AM, The decreasing prevalence of reversible dementias: an updated meta-analysis, Arch Int Med, 2003;163:2219–29.
  54. Michel JM, Sellal F, Reversible dementia in 2011, Geriatr Psychol Neuropsychiatr Vieil, 2011;9(2):211–25.
  55. Clarfield AM, Reversible dementia-the implications of a fall in prevalence, Age and Ageing, 2005;34:544–5.
  56. Hejl A, Hogh P, Waldemar G, Potentially reversible conditions in 1000 consecutive memory clinic patients, J Neurol Neurosurg Psychiatr, 2002;73(4):390–4.

Further Resources

Share this Article
Related Content In Alzheimer's Disease & Dementia
  • Copied to clipboard!
    accredited arrow-down-editablearrow-downarrow_leftarrow-right-bluearrow-right-dark-bluearrow-right-greenarrow-right-greyarrow-right-orangearrow-right-whitearrow-right-bluearrow-up-orangeavatarcalendarchevron-down consultant-pathologist-nurseconsultant-pathologistcrosscrossdownloademailexclaimationfeedbackfiltergraph-arrowinterviewslinkmdt_iconmenumore_dots nurse-consultantpadlock patient-advocate-pathologistpatient-consultantpatientperson pharmacist-nurseplay_buttonplay-colour-tmcplay-colourAsset 1podcastprinter scenerysearch share single-doctor social_facebooksocial_googleplussocial_instagramsocial_linkedin_altsocial_linkedin_altsocial_pinterestlogo-twitter-glyph-32social_youtubeshape-star (1)tick-bluetick-orangetick-red tick-whiteticktimetranscriptup-arrowwebinar Department Location NEW TMM Corporate Services Icons-07NEW TMM Corporate Services Icons-08NEW TMM Corporate Services Icons-09NEW TMM Corporate Services Icons-10NEW TMM Corporate Services Icons-11NEW TMM Corporate Services Icons-12Salary £ TMM-Corp-Site-Icons-01TMM-Corp-Site-Icons-02TMM-Corp-Site-Icons-03TMM-Corp-Site-Icons-04TMM-Corp-Site-Icons-05TMM-Corp-Site-Icons-06TMM-Corp-Site-Icons-07TMM-Corp-Site-Icons-08TMM-Corp-Site-Icons-09TMM-Corp-Site-Icons-10TMM-Corp-Site-Icons-11TMM-Corp-Site-Icons-12TMM-Corp-Site-Icons-13TMM-Corp-Site-Icons-14TMM-Corp-Site-Icons-15TMM-Corp-Site-Icons-16TMM-Corp-Site-Icons-17TMM-Corp-Site-Icons-18TMM-Corp-Site-Icons-19TMM-Corp-Site-Icons-20TMM-Corp-Site-Icons-21TMM-Corp-Site-Icons-22TMM-Corp-Site-Icons-23TMM-Corp-Site-Icons-24TMM-Corp-Site-Icons-25TMM-Corp-Site-Icons-26TMM-Corp-Site-Icons-27TMM-Corp-Site-Icons-28TMM-Corp-Site-Icons-29TMM-Corp-Site-Icons-30TMM-Corp-Site-Icons-31TMM-Corp-Site-Icons-32TMM-Corp-Site-Icons-33TMM-Corp-Site-Icons-34TMM-Corp-Site-Icons-35TMM-Corp-Site-Icons-36TMM-Corp-Site-Icons-37TMM-Corp-Site-Icons-38TMM-Corp-Site-Icons-39TMM-Corp-Site-Icons-40TMM-Corp-Site-Icons-41TMM-Corp-Site-Icons-42TMM-Corp-Site-Icons-43TMM-Corp-Site-Icons-44TMM-Corp-Site-Icons-45TMM-Corp-Site-Icons-46TMM-Corp-Site-Icons-47TMM-Corp-Site-Icons-48TMM-Corp-Site-Icons-49TMM-Corp-Site-Icons-50TMM-Corp-Site-Icons-51TMM-Corp-Site-Icons-52TMM-Corp-Site-Icons-53TMM-Corp-Site-Icons-54TMM-Corp-Site-Icons-55TMM-Corp-Site-Icons-56TMM-Corp-Site-Icons-57TMM-Corp-Site-Icons-58TMM-Corp-Site-Icons-59TMM-Corp-Site-Icons-60TMM-Corp-Site-Icons-61TMM-Corp-Site-Icons-62TMM-Corp-Site-Icons-63TMM-Corp-Site-Icons-64TMM-Corp-Site-Icons-65TMM-Corp-Site-Icons-66TMM-Corp-Site-Icons-67TMM-Corp-Site-Icons-68TMM-Corp-Site-Icons-69TMM-Corp-Site-Icons-70TMM-Corp-Site-Icons-71TMM-Corp-Site-Icons-72