Note that the most common cause of dementia by far is
Alzheimer’s disease. This is followed by
Lewy body dementia and mixed dementia. However, before categorizing a patient
into one of these categories, it is essential to rule out any treatable or
reversible causes of dementia as shown above in red.
Depression is very common in the elderly and may mimic dementia. This
may be revealed by directly asking the patient or caregiver whether they notice
any changes in mood, sleep patterns, appetite, inability to get pleasure from
previously pleasurable activities. Clinical testing will reveal a poor
concentration or frustration in answering the examiner’s questions. Often a
neuropsychological testing will help uncover depression.
Metabolic disorders, may mimic dementia. The most common of these
includes B12 deficiency
and hypothyroidism. B12 deficiency may occur s/p gastric bypass surgery due to
loss of intrinsic factor production. Pernicious anemia or malnutrition are other
causes. In addition to dementia, the patient may also have subacute combined
degeneration or peripheral neuropathy. Subacute combined degeneration is
weakness and imbalance due to degeneration of corticospinal tracts and posterior
columns respectively. The patient may have hyperreflexia on exam, weakness and
loss of propioceptive and vibratory sense. The diagnosis of B12 deficiency is
made by checking serum B12, homocysteine and methylmalonic acid (MMA) levels.
Hypothyroidism may present as dementia. Patients may have other signs of
hypothyroidism such as loss of energy, weight gain, hair loss, depression. Serum
TSH is a good screen. Free T4 and T3 may be checked as well.
Infections should be suspected in the presence of fever, leukocytosis.
The patient may have focal neurological findings with abscesses. Altered level
of consciousness may raise suspicion as this is not found in dementia. Risk
factors for HIV and syphilis should be sought. HIV and VDRL or RPR testing
should be done in suspected patients. Neuroimaging may be useful in revealing
abscess,
meningeal enhancement,
PML (in HIV). Lyme titers should be drawn
in patients living in tick endemic areas. Lumbar puncture may be diagnostic, but
should be done after neuroimaging to exclude a mass lesion. Although a
transmittable disease and not an infection in the traditional sense,
Creutzfeldt-Jakob disease is a rapidly progressive and fatal dementia caused
by abnormal prion proteins. In addition to cognitive changes, the patient
usually has some combination of ataxia, myoclonus, visual impairments and severe
sleep disturbances. Neuroimaging may show bright focal abnormalities in thalami
and basal ganglia. EEG may show periodic sharp waves complexes. CSF may show
elevated 14-3-3 protein. There is no treatment for CJD.
Structural lesions as a cause of dementia are uncommon, however should
be suspected if any focal neurologic signs
are discovered.
Meningioma is a slow growing benign tumor that may produce
gradual changes in cognitive function mimicking a dementia. Other tumors may
also produce dementia. MRI with gadolinium will reveal the mass lesion. Other
structural lesions include
chronic subdural hematoma. Risk factors
include anticoagulation with warfarin, falls, and elderly patients. CT head or
MRI usually detect this.
Alcoholic dementia should be suspected in patients with a history of
alcohol abuse. Any patient presenting with change in mental status should
receive IV thiamine to avoid precipitating Wernicke’s encephalopathy. The
etiology of alcoholic dementia is probably multifactorial, but probably involves
nutritional deficiency and/or direct toxic effect of alcohol. On exam, patients
may have ataxia due to vermal degeneration. A peripheral neuropathy is also
commonly present.
Hydrocephalus may mimic dementia.
Normal pressure hydrocephalus (NPH) is a
triad of: dementia, urinary incontinence and gait ataxia. Neuroimaging using CT
scan or MRI shows large ventricles out of proportion to cortical atrophy. LP
usually shows normal pressure, however continuous lumbar pressure monitoring
usually shows periodic rises in CSF pressure. Treatment of NPH involves CSF
shunting.
Alzheimer’s disease, the most common form of dementia is an insidious,
slowly progressive dementia. The hallmark is memory loss, usually starting with
short-term loss, then progressing to long-term. Multiple cognitive areas may be
affected including memory, naming, spatial abilities, language, praxis,
executive function. Personality is usually preserved until late in the disease.
Diagnosis is based on diagnostic criteria with exclusion of reversible causes.
Treatment is with acetylcholinesterase inhibitors such as donepezil,
rivastigmine or galantamine, however these do not stop the overall progression
of the disease. Vitamin E may have a marginal benefit, but newer studies
indicate a possible increase in cardiovascular risk. Memantine is a newly FDA
approved treatment that involves the blockade of glutamate that is thought to be
neurotoxic.
Lewy Body dementia is an underrecognized cause of dementia. The Lewy
body is a neuropathological entity that is associated with Parkinson’s disease.
Clinical features of Lewy body dementia include cognitive impairment, sleep
disturbance, fluctuating course, visual hallucinations, executive dysfunction.
There may be signs of Parkinson’s disease such as bradykinesia, tremor and
rigidity. Autonomic dysfunction is common (orthostatic hypotension, urinary
incontinence, constipation) Treatment with acetylcholesterase inhibitors and
memantine may be helpful. Symptomatic treatment of hallucinations, sleep
disturbances, parkinson’s features and dysautonomia are helpful.
Vascular dementia may be difficult to distinguish from Alzheimer’s
disease. A step-wise course related to repeated strokes may suggest vascular
dementia. A history of diabetes or HTN may raise suspicion for this form of
dementia. MRI may show multiple cerebral infarcts. The
Hachinski scale
may help differentiate vascular dementia from Alzheimer’s, although these two
entities may coexist. A score>7 indicates vascular dementia, whereas < 4
indicates Alzheimer’s disease. Treatment of vascular dementia is symptomatic
with acetylcholinesterase inhibitors and modification of vascular risk factors.
Frontotemporal dementia is a rare dementia that preferentially
involves frontal and temporal lobes. Onset may be < 65 years. Personality change
and emotional changes occur early in the disease. Executive dysfunction occurs
early. Altered speech production occurs early. Memory dysfunction does not occur
early on. Spatial orientation is usually preserved initially. Imaging shows
frontal lobe and temporal lobe atrophy out of proportion to parietal lobe and
other cortical areas. |
