How Reversible are ‘Reversible Dementias’? 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


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


However, many people with dementia present with abnormal thyroid tests in their blood tests or history.


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


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?


EUROPEAN NEUROLOGICAL REVIEW Toxic conditions Vitamin B12 deficiency may be an epiphenomenon


Table 1: Summary of Different Possible Causes (Traditional and New) of Reversible Dementias or Dementia-like Symptoms


Groups Diseases/Causative Agents Structural brain lesions NPH


Subdural haematomas Brain tumours


Alcoholic dementia Nutritional disorders


Endocrine disorders Metabolic disorders Vitamin B12 deficiency


Wernicke’s encephalopathy Hypothyroidism


Hyperthyroidism Hypoparathyroidism


Electrolyte disturbances Wilson’s disease


Serum B12 Thiamine


Serum T3, T4, TSH


Parathormone K+, Na+, Ca2+


Hepatic and renal insufficiency Hepatic enzymes, creatinine Copper,


ceruroplasmin


Obstructive sleep apnoea Poisoning with CO, bismuth, aluminium, manganese, arsenic, mercury


Psychiatric disorders Depression


Epileptic disorders Autoimmune


encephalopathies


Transient epileptic amnesia Hashimoto’s encephalopathy Paraneoplastic


encephalopathies


Inflammatory vasculopathies


Non-paraneoplastic encephalopathies Primary CNS angiitis


Sjögren syndrome SLE


Behçet’s disease CNS sarcoidosis


Antiphospholipid syndrome Vascular causative


factors Infections


Polysomnography History, serum levels


Psychometric tests


History, EEG


Anti-TPO, anti-TG Anti-Yo, anti-Ri, anti-Hu,


anti-NMDAR VGKC


Angiography, biopsy


Anti-Ro, anti-La Anti-dsDNA, ANA Oral, genital ulcers ACE


Lupus


anticoagulant, cardiolipines


Dural arteriovenous fistulae MRV Cryptococcal meningitis Whipple’s disease Lyme disease Syphilis HIV dementia Medications


Benzodiazepines, antiepileptics,


antipsychotics, tricyclic antidepressants


ACE = angiotensin-converting enzyme; ANA = antinuclear antibody; CNS = central nervous system; CO = carbon monoxide; CSF = cerebrospinal fluid; CT = computed tomography; EEG = electroencephalogram;


MRI = magnetic resonance imaging; MRV = magnetic resonance venography; NMDAR = N-methyl-d-aspartate receptor; NPH = normal pressure hydrocephalus; PCR = polymerase chain reaction; SLE = systemic lupus erythematosus;


TG = thyroglobulin; TPO = thyroid peroxidase; TSH = thyroid-stimulating hormone; VDRL = venereal disease research laboratory test; VGKC = voltage-gated potassium channel.


PCR for


Cryptococcus PCR for


Tropheryma whippelii


Serum and CSF antibodies for borellia


CSF for VDRL


Serology for HIV History, serum levels


Diagnostic Tests Brain CT, MRI


231


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